APRV1

�Airway pressure release ventilation(APRV) is a relatively new mode ofventilation, that only becamecommercially available in the UnitedStates in the mid-1990s. Airway pressurerelease ventilation produces tidalventilation using a method that differsfrom any other mode. It uses a release ofairway pressure from an elevatedbaseline to simulate expiration. Theelevated baseline facilitates oxygenation,and the timed releases aid in carbondioxide removal.

Advantages of APRV include lowerairway pressures, lower minuteventilation, minimal adverse effects oncardio-circulatory function, ability tospontaneously breathe throughout theentire ventilatory cycle, decreasedsedation use, and near elimination ofneuromuscular blockade. Airway pressurerelease ventilation is consistent with lungprotection strategies that strive to limitlung injury associated with mechanicalventilation. Future research will probablysupport the use of APRV as the primarymode of choice for patients with acutelung injury. (KEYWORDS: acute lunginjury, airway pressure releaseventilation, alveolar recruitment, alveolarderecruitment, lung protective strategies)

Airway pressure release ventilation (APRV) isa mode of ventilation that was first describedin 1987.1,2 It uses a philosophy that differsfundamentally from that of conventionalventilation. Whereas conventional modes of

AACN Clinical IssuesVolume 12, Number 2, pp. 234–246© 2001, AACN

ventilation begin the ventilatory cycle at abaseline pressure and elevate airway pres-sure to accomplish tidal ventilation (Figure1), APRV commences at an elevated baselinepressure (similar to a plateau pressure) andfollows with a deflation to accomplish tidalventilation (Figure 2). In addition, duringAPRV, spontaneous breathing may occur ateither the plateau pressure or deflation pres-sure levels. This article provides a detailedexamination of the terminology, indications,theoretical benefits, advantages, and disad-vantages of APRV as well as a discussion ofapplication and weaning procedures.

� Airway Pressure ReleaseVentilation Defined

Airway pressure release ventilation has beendescribed as continuous positive airway pres-sure (CPAP) with regular, brief, intermittentreleases in airway pressure.3,4 The releasephase results in alveolar ventilation and re-moval of carbon dioxide (CO2). Airway pres-sure release ventilation, unlike CPAP, facili-tates both oxygenation and CO2 clearanceand originally was described as an improvedmethod of ventilatory support in the presenceof acute lung injury (ALI) and inadequate CO2

ventilation.2,5 Airway pressure release ventila-tion is capable of either augmenting alveolar

Airway Pressure ReleaseVentilation: Theory and PracticeP. Milo Frawley, RN, MS,* and Nader M. Habashi, MD†

▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪ ▪

From *Maryland ExpressCare and †Department ofCritical Care Medicine, University of Maryland MedicalCenter, Baltimore, Maryland.

Reprint requests to P. Milo Frawley, RN, MS, Mary-land ExpressCare, TGR25C, University of MarylandMedical Center, 22 South Greene Street, Baltimore, MD21201.

234

Vol. 12, No. 2 May 2001 APRV: THEORY AND PRACTICE � 235

ventilation in the spontaneously breathing pa-tient or accomplishing complete ventilation inthe apneic patient.6 The CPAP level drivesoxygenation, while the timed releases aid inCO2 clearance.

Technically, APRV is a time-triggered, pres-sure-limited, time-cycled mode of mechanicalventilation. In addition, APRV allows unre-stricted, spontaneous breathing throughout

the entire ventilatory cycle (Table 1). Advan-tages of APRV include: significantly lowerpeak/plateau airway pressures for a giventidal volume; the ability to superimpose spon-taneous breathing throughout the ventilatorycycle; decreased sedation; and near elimina-tion of neuromuscular blockade use.7,8 Fea-tures that distinguish APRV from other modesof mechanical ventilation include sponta-

Figure 1. Conventional volume targeted ventilation, e.g., synchronized intermittent mandatory ventilation(SIMV). Any mechanically delivered breath will be defined by its trigger, limit, and cycle off feature. In SIMV, thebreath will be triggered by either the patient or by time, the volume delivered will limit the breath, and time will cy-cle the breath off into exhalation. Cms of H2O = centimeters of water.

Figure 2. Airway pressure release ventilation: this can also be defined by a trigger, limit, and cycle off feature.However, unlike other modes of ventilation, the trigger (time) initiates a drop in airway pressure. The amount ofpressure change will be the limit. The cycle off will occur because of time. Airway pressure then returns to thebaseline. Cms of H2O = centimeters of water.

236 � FRAWLEY AND HABASHI AACN Clinical Issues

neous breathing throughout the ventilatorycycle and an intermittent pressure releasephase that results in a brief decrease in lungvolume to assist ventilation.1,2

� History of MechanicalVentilation

The basic principles of ventilator design andmanagement were founded upon patientswho developed nonparenchymal respiratoryfailure (e.g., polio). In the absence of ade-quate research, those same principles wereapplied to patients with parenchymal respira-tory failure as well (e.g., ALI). Mode selectionoften was based on availability and simplicityof the ventilator, user experience, and tradi-tion, because little evidence existed to guidemanagement.

In 1993, the American College of ChestPhysicians (ACCP) consensus conferencefailed to “agree on an optimum mode ofventilation for any disease state or an opti-mum method of weaning patients from me-chanical ventilation.”9(p1834) The ACCPagreed that well-controlled clinical trialsthat defined the indications and uses ofspecific modes of ventilation were lacking.New technology must scientifically show adistinct advantage in safety, expense, easeof operation, or therapeutic outcome.10,11

Despite more than 30 years since itsrecognition, acute respiratory distress syn-drome (ARDS) continues to have a 30% to50% mortality rate.12,13 Recently, discovery ofthe potential for mechanical ventilation toproduce ventilator-associated lung injury hasresulted in the development of new lungprotective strategies.14 Lung protective strate-gies include those described in the “theopen lung approach” promoted by Amato etal.15 The open lung approach uses reducedtidal volumes (6 mL/kg) to prevent high-vol-ume lung injury and over-distension of air-spaces. In addition, Amato et al.16 used ele-vated end expiratory pressure (averagepositive end-expiratory pressure [PEEP] 16cm water pressure), to prevent low volumelung injury from cyclic airway reopening.

The recently completed ARDSNet studycompared conventional tidal volume (12mL/kg) to reduced tidal volume (6 mL/kg).13

The results of the ARDSNet trial13 and astudy conducted by Amato et al.16 suggest anassociation between reduced tidal volumeand improved outcome. Although the ARD-SNet trial targeted similar PEEP levels in bothits groups, study protocols for maintainingsaturation resulted in higher levels of setPEEP in the low tidal volume group. In addi-tion, to maintain similar targets for PaCO2,the low tidal volume group had much higherrespiratory frequencies, resulting in the de-

TABLE 1 � Classification of Common Modes of Mechanical Ventilation

SpontaneousMode Trigger Limit Cycle Off Breathing Flow of Gas

A-C Time or patient Volume Time No Constant(volume)

A-C Time or patient Pressure Time No Decelerating(pressure)

SIMV Time or patient Volume Time Yes Constant(volume)

PSV Patient Pressure Flow of gas No Decelerating

PRVC Time or patient* Volume Time No Decelerating

APRV Time Pressure Time Yes Decelerating

Note: A mechanically delivered breath is made up of three distinct phases. The Trigger initiates the breath; the Limit will stop thebreath from increasing, but does not initiate exhalation; and the Cycle Off, that switches the breath from inspiration to exhala-tion. Beyond this, modes may or may not allow unsupported, spontaneous breathing. The inspired gas may be delivered usingeither a constant or decelerating flow of gas.

*This mode is designed for patients with no breathing capacity, though they are able to trigger breaths.

A-C � assist control; SIMV � synchronized intermittent mandatory ventilation; PSV � pressure support ventilation; PRVC � pressure regulated volume control; APRV � airway pressure release ventilation.


velopment of intrinsic PEEP. Therefore, therole of elevated levels of end expiratorypressure (PEEP) on survival of the low tidalvolume group may have been obscured. De-spite improved survival with the low tidalvolumes group, survival was less than that ofAmato’s16 combined approach (tidal volumereduction and PEEP elevation). As a result,the planned ARDSNet Assessment of Lowtidal Volume and Elevated end-expiratoryvolume to Obviate Lung Injury (ALVEOLI)study will evaluate the role of higher levelsof PEEP on survival. ARDSNet ALVEOLI willuse data from the pressure-volume curve todevelop the PEEP scale (PEEP scale = frac-tion of inspired oxygen:PEEP).

However, recent data suggest that deter-mining optimal PEEP from the pressure-vol-ume curve may be inaccurate.17 In addition,recruitment to prevent cyclic airway closure(low volume lung injury) requires pressurein excess of 30 cm of water pressure. Com-plete recruitment exceeds the lower inflec-tion point used by Amato et al.16 to deter-mine optimal PEEP levels. Recruitmentbegins at the lower inflection point andcontinues to the upper inflection point.18–20

Therefore, elevated baseline airway pres-sure during APRV may produce near com-plete recruitment, thus minimizing low vol-ume lung injury from cyclic recruitment.Additionally, APRV is less likely to produceover-inflation or high-volume lung injury,as airway pressures are lowered (released)to accomplish ventilation.

Other lung protective strategies includeoptimization of current modes of ventilationand alteration of ventilator strategies to pre-vent or reduce ventilator-associated lung in-jury. Current goals of ventilation include thefollowing:

• avoiding extension of lung injury,• minimizing oxygen toxicity by using

mean airway pressure (Paw),• recruiting alveoli by raising mean Paw by in-

creasing PEEP and/or prolonging inspira-tion,

• minimizing peak Paw,• preventing atelectasis, and• using sedation and paralysis judiciously.21

Although first described 11 years earlier,1,2

APRV may have benefits for preventing orlimiting ventilator-associated lung injury.

� Terminology

Unfortunately, a consistent vocabulary forAPRV has failed to mature. Four commonlyused terms include: pressure high (P High),pressure low (P Low), time high (T High),and time low (T Low).7 P High is the baselineairway pressure level and is the higher of thetwo airway pressure levels. Other authorshave described P High as the CPAP level,22

the inflating pressure,23 or the P1 pressure(P1). P Low is the airway pressure level re-sulting from the pressure release. Other au-thors may refer to P Low as the PEEP level,22

the release pressure,23 or the P2 pressure(P2). T High corresponds with the length oftime for which P High is maintained; T Lowis the length of time for which the P Low isheld (i.e. for which the airway pressure is re-leased).

The mean airway pressure can be calcu-lated as follows:7

(P High � T High) + (P Low � T Low)

T High + T Low

Some ventilators may compute this auto-matically, making manual calculation redun-dant. Common terms associated with APRVare summarized in Table 2 and Figure 3.

Somewhat confusing to the understand-ing of APRV have been the subsequent de-scriptions of modes of ventilation that ap-pear very similar to it. Biphasic positiveairway pressure (BIPAP)24,25 differs fromAPRV only in the timing of the upper andlower pressure levels. In BIPAP, T High usu-ally is shorter than T Low. One descriptionof BIPAP25 subdivides it into four categories,one of which is APRV-BIPAP.

Intermittent mandatory pressure releaseventilation (IMPRV),26 another mode of ven-tilation similar to and sometimes confusedwith APRV, synchronizes the release eventwith the patient’s spontaneous effort. The re-lease occurs after the patient’s second, third,fourth, fifth, or sixth spontaneous breath.Further, all spontaneous breaths are pressuresupported to overcome the resistance associ-ated with breathing through the endotra-cheal tube and ventilator tubing. Synchro-nization does not occur with the raising ofairway pressure, only the release. Becausethe concept of dyssynchrony in APRV hasnot been demonstrated clearly—and has


Figure 3. Airway pressure release ventilation terminology. Paw = airway pressure; P High = 30 centimeters of wa-ter (cms of H2O); P Low = 0 cms of H2O, T High = 6.0 seconds; T low = 0.8 seconds; calculated mean Paw = 26.5cms of H2O.

BiLevel ventilation28 is defined as aug-mented pressure ventilation that allows forunrestricted, albeit pressure-supported, spon-taneous breathing throughout the ventilatorycycle. Although similar to APRV, it incorpo-rates the option of pressure support in the air-way pressure waveform to augment sponta-neous breathing.

� Indications for APRV

Airway pressure release ventilation was de-signed to oxygenate and augment ventila-tion for patients with ALI or low-compliance

been stated not to be an issue—the necessityof intermittent mandatory pressure releaseventilation is questionable.10

Intermittent CPAP27 is based on the prin-ciples of APRV but is intended for patientsundergoing general anesthesia. Continuouspositive airway pressure is applied at alevel that will provide an adequate tidalvolume, then removed for 1 second to pro-duce tidal ventilation, then reapplied. Un-like APRV, intermittent CPAP is not in-tended to restore normal functional residualcapacity or improve oxygenation, and it canbe discontinued abruptly.

TABLE 2 � Summary of Airway Pressure Release Ventilation Terminology

Alternative Units of Term Definition Names Measure

Pressure High Baseline airway pressure level CPAP level,22 Cm H2O(P High)7 Higher of the two airway pressures Inflation pressure,23 P1

Pressure Low Airway pressure level resulting from PEEP level,22 Release Cm H2O(P Low)7 pressure release. The lower of the two pressure,23 P2

airway pressures

Time High Length of time for which P High is T1 Seconds(T High)7 maintained

Time Low Length of time for which P Low is T2 Seconds(T Low)7 maintained

Mean Paw (P High � T High) � (P Low � T Low) — Cm H2O

(T High � T Low)7

CPAP � continuous positive airway pressure; Cm H2O � centimeters of water; PEEP � positive end expiratory pressure; Paw � airway pressure.


lung disease.1,5,6 Airway pressure releaseventilation also has been used successfullywith patients with airway disease. Similar toCPAP, APRV can unload inspiratory musclesand decrease the work of breathing associ-ated with chronic obstructive pulmonary dis-ease.29 Unlike PEEP (an expiratory flow re-sistor, which decreases expiratory flow),peak expiratory flow rates are increased dur-ing the release phase of APRV, improvingexpiratory flow limitation. Furthermore, dur-ing APRV, exhalation is not limited to the re-lease phase, as it is permitted throughout therespiratory cycle.

The main causes of hypoxemia associ-ated with ALI are shunting due to alveolarcollapse and reduction in functional resid-ual capacity.1,7,30 Therefore, a primary goalof the treatment of ALI is recruitment ofalveoli and prevention of derecruitment.Sustained plateau pressure is used to pro-mote alveolar recruitment, while beingmaintained at an acceptable level. In addi-tion, the number of respiratory cycles isminimized to prevent both the repetitiveopening of alveoli and alveolar stretch, thatmay result in lung injury.

Patients in early-phase ALI often do nothave impaired respiratory muscle strength orinadequate respiratory drive. Frequently,CPAP alone is sufficient to restore lung vol-ume and increase lung compliance. How-ever, when assistance with ventilation is re-quired, APRV can be used. Intermittent

airway pressure release allows alveolar gasto be expelled via natural lung recoil.1

� Importance of CollateralChannels of Ventilation

Maintaining a constant airway pressure maybe advantageous for several reasons. Con-stant airway pressure facilitates alveolar re-cruitment; enhances diffusion of gases; al-lows alveolar units with slow time constantsto fill, preventing over-distension of alveoli;and augments collateral ventilation.31

Van Allen et al32 noted that complete ob-struction of an airway unit did not always re-sult in collapse of the alveoli and, therefore,hypothesized that alternative pathways mustexist. The pores of Kohn, located in the septaof the alveoli and open only during inspira-tion,33 first were believed to be responsible.However, two additional pathways were latercredited with playing a role: (1) Lambert’scanals connect terminal and respiratory bron-chioles with adjacent peribronchial alveoli,and (2) channels of Martin interconnect respi-ratory bronchioles and serve to bypass themain pathway (Figure 4).34

In normal, healthy lungs, collateral venti-lation may barely occur at the functionalresidual capacity level, i.e. end exhalation.However, alternative pathways may beopened at a higher lung volume.35 The roleof alternative pathways in healthy lungs isvery limited; but in disease states may be im-

Figure 4. Collateral channels of ventilation.


portant.36 Although collateral ventilation istypically lost in pulmonary edema, collateralpathways may be reopened and oxygena-tion improved by increasing functional resid-ual capacity.36 Sustained airway pressure,rather than intermittent periods of airwaypressure, is more beneficial in the edema-tous, collapsed lung. Sustained breathsmaintain a constant airway pressure and al-low collateral channels to assist in producingventilation. Collateral ventilation efficiencydrops as respiratory frequency increases.37

Airway pressure release ventilation usesthese concepts, maintaining sufficient airwaypressure for an adequate duration to opencollapsed alveoli, thus improving recruit-ment of alveoli and increasing oxygenation.

� Advantages

In patients with severe acute respiratory fail-ure, the use of APRV results in significantlylower peak Paw, when compared with con-tinuous positive pressure ventilation (CPPV).Lower airway pressures are thought to be as-sociated with a reduced risk of ventilator-as-sociated lung injury.14 Further, APRV re-quires lower minute ventilation than CPPV,suggesting less dead-space ventilation.23

Studies of patients with ALI have shown thatAPRV supports oxygenation and ventilation,while producing lower peak Paw than volumeassist-control ventilation5 and intermittentmandatory ventilation.8,11 Similarly, animalstudies of injured lungs suggest lower airwaypressure, reduced dead space ventilation,and improved oxygenation and ventilation,when compared with intermittent positivepressure ventilation.2

Airway pressure release ventilation re-cruits lung units by optimizing end-inspira-tory lung volume. Ideally, the end-inspira-tory pressure, which equates to P High orplateau pressure, should be kept beneath 35cm of water pressure.9 This protective lungstrategy has several positive effects. First, thepreset pressure limit prevents, or limits,over-distension of alveoli and high-volumelung injury. Second, APRV affects tidal venti-lation by decreasing rather than increasingairway pressure. Decreasing lung volume forventilation further limits air space over-dis-tension and the potential for high-volume

lung injury. Third, maintaining airway pres-sure optimizes recruitment and prevents orlimits low-volume lung injury by avoidingthe repetitious opening of alveoli.14

High-volume lung injury occurs as a re-sult of tidal ventilation above the upper in-flection point of the pressure-volume curve.Low-volume lung injury results from ventila-tion beginning beneath the lower inflectionpoint.17 Airway pressure release ventilationbegins on the pressure-volume curve be-tween these two points and uses a release,not an increase, of pressure from its base-line. Therefore, oxygenation and ventilationoccur predominantly within the upper andlower inflection points (Figure 5).

Calzia and Radermacher,38 in their 10-yearliterature review of APRV, were unable todocument any severe adverse effects ofAPRV and BIPAP on cardio-circulatory func-tion. One case report39 demonstrated an in-crease in cardiac output and blood pressurewhen APRV was used. Further, the authorssuggested that it should be considered as analternative therapy to pharmacologic or fluidtherapy in the hemodynamically compro-mised, mechanically ventilated patient.

Animal studies indicate that APRV doesnot compromise circulatory function and tis-sue oxygenation, whereas CPPV can impaircardiovascular function significantly.40 Spon-taneous ventilation has a positive effect onthe venous thoracic pump mechanism. Sup-pressing spontaneous breathing during CPPVcan compromise cardiac function by decreas-ing venous return, thus cardiac output.4

The main advantage of APRV is that it al-lows for spontaneous breathing to occur atany point in the respiratory cycle. Depend-ing on the patient’s need, spontaneousbreathing may involve only exhalation, onlyinspiration, or both.

The distribution of ventilation is signifi-cantly different when a spontaneous breathis compared with a mechanically controlledor assisted breath. Spontaneous breaths tendto improve ventilation-perfusion matchingby preferentially aerating well-perfused, de-pendent lung regions. Mechanically deliv-ered breaths primarily ventilate areas awayfrom those receiving maximal blood flow.This phenomenon is consistent with earlierresearch, which demonstrated that sponta-neous ventilation opens more alveoli, im-


proves regional gas exchange, and reducesatelectasis.41

Putensen et al.42,43 found that by allowingunsupported, spontaneous breathing (usingBIPAP or APRV) in both dogs42 and humans43

with ALI, ventilation-perfusion matching im-proved, as seen by a marked decrease in in-trapulmonary shunt. In humans, however,pressure support ventilation preferentiallyventilated poorly or nonperfused lung unitsthat already were well ventilated. Further-more, pressure support ventilation did notconvert shunted areas to normal ventilation-perfusion units.43

Decreased need for sedation use or neuro-muscular blockade use with APRV7,8 and BI-PAP25 has been reported. Judicious use of se-dation and paralysis in the mechanicallyventilated patient was recommended at theAmerican-European Consensus Conference onARDS.21 Unintentional, prolonged paralysis isnow recognized as a complication of the long-term use of paralytics. In addition, a paralyzeddiaphragm moves very differently with posi-tive pressure ventilation compared with an ac-tive contraction. The paralyzed diaphragm isdisplaced preferentially along the path of leastresistance, that is, into the abdomen of the nondependent region. This displacement leads tofavored ventilation of the nondependent lung

regions.41 All of this contributes to both ventila-tion-perfusion mismatch and possible over-dis-tension of healthy alveoli, leading to furtherhypoxemia (Table 3).

� Disadvantages

Consistent with other pressure-targetedmodes of ventilation, APRV is affected bychanges in lung compliance and/or resis-tance. Clinicians need to identify the scenar-ios that affect lung volume and monitor pa-tients for changes in their tidal volumes.

Because APRV is time-cycled, synchronywith the patient’s spontaneous respirationdoes not occur. If a release phase is not syn-chronous with the patient’s effort, discomfortmay result. However, because APRV has a dy-namic pneumatic system, inspiration and exha-lation are facilitated at any time. Dyssynchronywith APRV has not been identified as a prob-lem in the majority of the literature to date.5,6,11

As with any new technology, staff stressand subsequent increased risk to the patientmay be noted with the implementation ofAPRV. Adequate and appropriate on-site train-ing, coupled with off-site support services andbackup, will help resolve some of the stressand decrease the risks associated with the in-

Figure 5. Pressure-volume curve. Conceptual drawing of airway pressure release ventilation occurring below theupper inflection point and above the lower inflection point, achieving goals of lung protective strategies.


troduction of APRV. Transferring patients tosubacute areas as their disease processes im-prove, may cause these issues to be revisited.Further, these areas may not have access toventilators capable of delivering APRV, whichwill require switching the patient to a differentmode of ventilation. Similarly, traveling toother departments (e.g., radiology, hyperbaricoxygenation chamber) may require temporarydiscontinuation of APRV, causing undue anxi-ety or discomfort in some patients.

Finally, only limited research exists re-garding the clinical practice of APRV and itscomparison with other modes. For example,APRV is suitable for ventilator weaning,though its superiority to mainstream modes,e.g. pressure support ventilation, has notbeen demonstrated. Weaning, in general,lacks a consensus, and this absence of ab-solutes exemplifies the great confusionwithin clinical practice and within the studyof mechanical ventilation (Table 3).

� Application of APRV

Little direction on the application of APRV canbe found in the literature, other than as sug-gested by vendors and limited study proto-cols. However, based on an understanding ofpulmonary physiology and pathophysiology,coupled with the theoretical understanding ofmechanical ventilation44 and current recom-mendations from consensus conferences,9,21

the following technique has evolved.When changing a patient’s mode of venti-

lation to APRV, the initial settings are partlydeduced from values of conventional ventila-tion. The clinician converts the plateau pres-sure of the conventional mode to P High andseeks an expired minute ventilation of 2 to 3L/minute, less than when on conventionalventilation. This is accomplished by setting PHigh at the plateau pressure, with a ceilinglevel for the P High normally at 35 cm of wa-ter pressure. P Low is set at 0 cm of waterpressure. A P Low of zero produces minimalexpiratory resistance, thus accelerating expi-ratory flow rates, facilitating rapid pressuredrops. T High is set at a minimum of 4.0 sec-onds. A T High of less than 4.0 seconds be-gins to impact mean Paw negatively. T Low isset between 0.5 and 1.0 seconds (often at 0.8seconds). With these settings (P High = 35 cmof water pressure, P Low = 0 cm of water

pressure, T High = 4.0 seconds, T Low = 0.8seconds), the mean Paw will equal 29.2 cm ofwater pressure. It is not possible for conven-tional volume targeted modes to maintain amean Paw of 29 cm of water pressure and limitthe peak or plateau pressures to 35 cm of wa-ter pressure, and still produce sufficient tidalventilation.44

Application of APRV to newly intubatedpatients usually involves using standard pa-rameters and adjusting the settings accord-ingly. Commonly, in the patient with moder-ate to severe ALI we default to P High/P Lowof 35/0 cm of water pressure and T High/TLow of 4.0/0.8 seconds and allow sponta-neous breathing to take place.44

When attempting to avoid alveolar over-distension, the clinician must be cognizantof the plateau pressure, as this is the bestclinically available estimate of average alveo-lar pressure.9 Although based primarily onanimal data, a plateau pressure (or P High)greater than 35 cm of water pressure is asso-ciated with lung injury and, therefore,should be kept beneath this level.

Rarely, an elevated P High (40–45 cm ofwater pressure) may be indicated, especially

TABLE 3 � Advantages and Potential Disadvantagesof Airway Pressure Release Ventilation

AAddvvaannttaaggeess

1. Lower Paw for a given tidal volume comparedwith volume-targeted modes, e.g., AC, SIMV

2. Lower minute ventilation, i.e., less dead spaceventilation

3. Limited adverse effects on cardio-circulatoryfunction

4. Spontaneous breathing possible throughoutentire ventilatory cycle

5. Decreased sedation use6. Near elimination of neuromuscular blockade

usePPootteennttiiaall DDiissaaddvvaannttaaggeess

1. Volumes change with alteration in lungcompliance and resistance

2. Process of integrating new technology3. Limited access to technology capable of

delivering APRV4. Limited research and clinical experience

Paw � airway pressure; A-C � assist control; SIMV � synchronized intermittent mandatory ventilation; APRV � airway pressure release ventilation.


for patients with low-compliance respiratorysystems, (e.g., individuals with morbid obe-sity, abdominal distension, or chest walledema), either for the purpose of oxygena-tion or ventilation.44 Although not optimal,the increased P High would be less than thepressure generated by conventional modesto produce a similar response.22

The P Low of zero is selected because min-imal resistance to exhalation is the goal.Higher pressures may impede expiratory gasflow during passive lung recoil. The validconcern of collapsing alveoli with a P Low ofzero is negated with the use of a short T Low(0.5–0.8 seconds) to maintain end expiratorylung volume.

The minimum T High duration is 4.0 sec-onds. The goal is to create a nearly continu-ous airway pressure level, which serves torecruit collapsed alveoli and maintain re-cruitment, thus optimizing oxygenation andcompliance. As a patient’s lung mechanicsimprove, T High is progressively lengthenedto 12 to 15 seconds, usually in 0.5 to 2.0 sec-ond increments.44 A further advantage of thelong T High is the reduction in the numberof opening and closings of the small airways,one of the mechanisms implicated in the de-velopment of iatrogenic ALI.14

The T Low probably is the most closelystudied of the 4 parameters. Early writings5,22

suggested a T Low of 1.5 seconds as thenorm, which allows for complete emptying ofthe lungs. A longer T Low (3.0–4.0 seconds)in animals with ALI was associated with a de-crease in arterial oxygenation and the accu-mulation of hemorrhagic fluid in the endotra-cheal tube.5 An excessively long T Lowencourages alveolar derecruitment, atelecta-sis, and airway closure during the releasephase. Alternatively, an insufficient T Low po-tentially may result in inadequate exhalation,leading to dead space ventilation, hypercap-nia, and hemodynamic compromise.45 In-deed, an appropriately timed T Low is vital.44

Optimal release time allows for adequateventilation while minimizing lung volumeloss. Essentially, release time should impedecomplete exhalation in the slower compart-ments of the lung (i.e., areas of high compli-ance or high resistance to exhalation) andgenerate regional intrinsic PEEP. Theoreti-cally, this will enhance alveolar recruitment.4,7

Calculation of T Low depends on expira-tory time constants (T), which are a productof the compliance of the respiratory system(CRS) and the resistance of the airways(RAW); that is, T = CRS � RAW.4,45 Low-compli-

Figure 6. Inspiratory and expiratory flow of gas in airway pressure release ventilation.44 In this example, T Lowterminates at 40% of the peak expiratory gas flow. Baseline airway pressure is then rapidly re-established. T High= 6.0 seconds; T Low = 0.8 seconds.


ance states, such as ARDS, will have lower(or shorter) expiratory time constants andtherefore a lower (or shorter) T Low. Highresistance diseases, such as asthma, willhave longer time constants and requirelonger release times.45 Determining the cor-rect multiple of time constants to calculate TLow is a challenge of future research.

In practice, however, the clinician does notcalculate the time constants for each patient,but rather relies on an approximation of therestriction of expiratory flow, as indicated bythe expiratory flow of gas waveform (Figure6). When expiratory flow falls to approxi-mately 25% to 50% of peak expiratory flow,the clinician stops the release time and allowsthe airway pressure to return to P High.44

The transition to APRV may not result ininstant improvement in oxygenation. Consis-tent with observations of inverse ratio venti-lation,4 the positive effects may take severalhours to be realized. It appears that the re-cruitment of alveoli occurs “one by one.”Sydow et al.7 demonstrated that the maximalbeneficial effect of APRV upon oxygenationoccurred 8 hours after implementation, withno further improvement after 16 hours. Inearlier studies, data were collected withinthe first 60 minutes after transition to APRVand thus the full effect of time on alveolarrecruitment was not appreciated.

� Weaning From APRV

The current technique of weaning from APRVis guided by general principles of weaningused in clinical practice today. Knowledge ofthe signs of respiratory failure, as well as exclu-sion or correction of contributing factors pre-venting successful weaning, such as excessivesecretions, bronchospasm, sepsis, anxiety, anddiameter of endotracheal tubes and other deadspace devices, are paramount. The approachin APRV is to maintain lung volume, improvingboth oxygenation and ventilation. As such,rarely does a specific point in time occur whenweaning is “officially” commenced.

Primarily, the method to reduce support isthrough manipulation of P High and T High. PHigh will be lowered 2 to 3 cm of water pres-sure at a time, and T High will be lengthenedin 0.5- to 2.0-second increments, dependingon patient tolerance. The goal is to arrive atstraight CPAP—usually at 12 cm of water pres-sure—and then the clinician either weansCPAP or simply extubates the patient at 6 to 12cm of water pressure. Before switching toCPAP, P High often is approximately 14 to 16cm of water pressure and T High is at 12 to 15seconds (Table 4).44 Patients with more severeforms of ALI or ARDS are weaned on a slowerbasis. Changes in mean Paw are monitoredclosely for their effect on oxygenation. Simi-

TABLE 4 � Example of Airway Pressure Release Ventilation Settings in an Uncomplicated Case of Acute Lung Injury43*

Calculated MeanP High T High P Low T Low Airway Pressure

(cm H2O) (seconds) (cm H2O) (seconds) (cm H2O)

35 4.0 0 0.8 29.2

33 4.5 0 0.8 28.0

30 5.0 0 0.8 25.9

28 5.5 0 0.8 24.4

26 6.0 0 0.8 22.9

23 7.0 0 0.8 20.6

20 8.0 0 0.8 18.2

18 10.0 0 0.8 16.7

15 12.0 0 0.8 14.1

*Following the final settings, the patient was transitioned to CPAP of 12 cm of water pressure.

CPAP � continuous positive airway pressure; Cm H2O � centimeters of water; P High � pressure high; T High � time high; Plow � pressure low; T low � time low.


larly, exhaled minute ventilation is tracked inconjunction with CO2 removal.

� Conclusion

Airway pressure release ventilation canmaintain oxygenation and ventilation at alevel comparable to CPPV. Airway pressurerelease ventilation is associated with signifi-cantly lower peak airway pressures anddead space ventilation. Airway pressure re-lease ventilation uses almost constant airwaypressure that not only facilitates alveolar re-cruitment but also sustains that recruitmentonce it has occurred. Spontaneous, unsup-ported breathing during APRV may occur atany point in the ventilatory cycle. Sponta-neous breathing is advantageous because itdecreases intrapulmonary shunting and im-proves venous return. The ability to avoidneuromuscular blockade and decreased useof sedation have resulted in fewer complica-tions and decreased drug costs. Finally, ven-tilator-associated lung injury, which can re-sult from both high- and low-volume lungventilation, may be balanced and averted.

Few clinicians believe that any single, iso-lated treatment can be responsible for a ma-jor improvement in the outcome for patientswith ARDS. Combination therapy is expectedto be the standard, including such conceptsas prone positioning and permissive hyper-capnia. Part of that therapy may include theventilator strategy of APRV, which incorpo-rates the advantages listed above. The au-thors believe that future research will supportthe use of APRV as the mode of choice forpatients with ALI and ARDS.

Acknowledgments

The authors thank Jill Kuramoto for her sug-gestions and constructive criticism, and KrisDorman for reviewing the manuscript.

References1. Downs JB, Stock MC. Airway pressure release

ventilation: a new concept in ventilatory sup-port. Crit Care Med. 1987;15:459–461.

2. Stock MC, Downs JB, Frolicher D. Airwaypressure release ventilation. Crit Care Med.1987;15:462–466.

3. Rasanen J. Airway pressure release ventila-tion. In: Tobin MJ, ed. Principles and Practice

of Mechanical Ventilation. New York: Mc-Graw-Hill, Inc.; 1994:341–348.

4. Burchardi H. New strategies in mechanicalventilation for acute lung injury. Eur Respir J.1996;9:1063–1072.

5. Stock MC, Downs JB. Airway pressure releaseventilation: a new approach to ventilatorysupport during acute lung injury. Respir CareClin N Am. 1987;32:517–524.

6. Garner W, Downs JB, Stock MC, Rasanen J.Airway pressure release ventilation (APRV): ahuman trial. Chest. 1988;94:779–781.

7. Sydow M, Burchardi H, Ephraim E, ZielmannS, Crozier TA. Long-term effects of two differ-ent ventilatory modes on oxygenation inacute lung injury: comparison of airway pres-sure release ventilation and volume-controlled inverse ratio ventilation. Am JRespir Crit Care Med. 1994;149:1550–1556.

8. Davis K, Johnson DJ, Branson RD, CampbellRS, Johannigman JA, Porembka D. Airwaypressure release ventilation. Arch Surg. 1993;128:1348–1352.

9. Slutsky AS (chairman). ACCP consensus con-ference: mechanical ventilation. Chest. 1993;104:1833–1859.

10. Rasanen J. IMPRV: Synchronized APRV, ormore [editorial]? Intensive Care Med. 1992;18:65–66.

11. Rasanen J, Cane RD, Downs JB, et al. Airwaypressure release ventilation during acute lunginjury: a prospective multicenter trial. CritCare Med. 1991;19:1234–1241.

12. Milberg JA, Davis DR, Stienberg KP, HudsonLD. Improved survival of patients withacute respiratory distress syndrome (ARDS):1983–1993. JAMA. 1995;273:306–309.

13. Brower RG, Matthay MA, Morris A, et al. Ven-tilation with lower tidal volumes as comparedwith traditional tidal volumes for acute lunginjury and the acute respiratory distress syn-drome. N Engl J Med. 2000;342:1301–1308.

14. Dreyfuss D, Saumon G. Ventilator-inducedlung injury: lessons from experimental stud-ies. Am J Respir Crit Care Med. 1998;157:294–323.

15. Amato MBP, Barbas CSV, Medeiros DM, et al.Beneficial effects of the “open lung ap-proach” with low distending pressures inacute respiratory distress syndrome: aprospective randomized study on mechanicalventilation. Am J Respir Crit Care Med. 1995;152:1835–1846.

16. Amato MBP, Barbas CSV, Medeiros DM, et al.Effect of a protective-ventilation strategy onmortality in the acute respiratory distress syn-drome. N Engl J Med. 1998;338:347–354.

17. Hickling KG. The pressure-volume curve isgreatly modified by recruitment: a mathemat-


ical model of ARDS lungs. Am J Respir CritCare Med. 1998;158:194–202.

18. Jonson B, Richard J-C, Straus C, Mancebo J,Lemaire R, Brochard L. Pressure-volumecurves and compliance in acute lung injury:evidence of recruitment above the lower in-flection point. Am J Respir Crit Care Med.1999;159:1172–1178.

19. Gattinoni L, Pelosi P, Crotti S, Valenza F. Ef-fects of positive end-expiratory pressure onregional distribution of tidal volume and re-cruitment in adult respiratory distress syn-drome. Am J Respir Crit Care Med. 1995;151:1807–1814.

20. Carney DE, Bredenberg CE, Schiller HJ, et al.The mechanism of lung volume change dur-ing mechanical ventilation. Am J Respir CritCare Med. 1999;160:1697–1702.

21. Artigas A, Bernard GR, Carlet J, et al. TheAmerican-European consensus conferenceon ARDS, part 2: ventilatory, pharmacologic,supportive therapy, study design strategiesand issues related to recovery and remodel-ing. Intensive Care Med. 1998;24:378–398.

22. Valentine DD, Hammond MD, Downs JB,Sears NJ, Sims WR. Distribution of ventilationand perfusion with different modes of me-chanical ventilation. Am Rev Respir Dis. 1991;143:1262–1266.

23. Cane RD, Peruzzi WT, Shapiro BA. Airwaypressure release ventilation in severe acuterespiratory failure. Chest. 1991;100:460–463

24. Baum M, Benzer H, Putensen C, Koller W,Putz G. Biphasic positive airway pressure (BI-PAP): a new form of assisted ventilation.Anaesthesist. 1989;38:432–458.

25. Hormann C, Baum M, Putensen C, Mutz NJ,Benzer H. Biphasic positive airway pressure(BIPAP): a new mode of ventilatory support.Eur J Anaesthesiol. 1994;11:37–42.

26. Rouby JJ, Ben Ameur M, Jawish D, et al. Con-tinuous positive airway pressure (CPAP) vs.intermittent mandatory pressure release ven-tilation (IMPRV) in patients with acute respi-ratory failure. Intensive Care Med. 1992;18:69–75.

27. Bratzke E, Downs JB, Smith RA. IntermittentCPAP: a new mode of ventilation during gen-eral anesthesia. Anesthesiology. 1998;89:334–340.

28. Puritan Bennett Company. Two ventilatingstrategies in one mode: BiLevel. St. Louis,MO: Puritan Bennett Company; 1999.

29. Petrof BJ, Legare M, Goldberg P, Milic-Emili J,Gottfried SB. Continuous positive airwaypressure reduces work of breathing and dys-pnea during weaning from mechanical venti-lation in severe chronic obstructive pul-monary disease. Am Rev Respir Dis. 1990;141:281–289.

30. Smith RA, Smith DB. Does airway pressurerelease ventilation alter lung function afteracute lung injury? Chest. 1995;107:805–808.

31. Davis K Jr., Branson RD, Campbell RS,Porembka DT. Comparison of volume con-trol and pressure control ventilation: is flowwaveform the difference? J Trauma. 1996;41: 808–814.

32. Van Allen CM, Lindskog GE, Richter, HG. Col-lateral respiration: Transfer of air collaterallybetween pulmonary lobules. J Clinical Invest.1941;10:559.

33. Brashers VL, Davey SS. Alterations of pul-monary functions. In: McCance KL, HuetherSE, eds. Pathophysiology: The Biologic Basisfor Disease in Adults and Children. 3rd ed. StLouis, MO; Mosby; 1998:1165–1166.

34. Corrin B. Pathology of the Lungs. New York,NY: Churchill Livingstone; 2000:4.

35. Terry PB, Traystman RJ, Newball HH, BatraG, Menkes HA. Collateral ventilation in man.N Engl J Med. 1978;298:10–15.

36. Delaunois L. Anatomy and physiology of col-lateral respiratory pathways. Eur Respir J. 1989;2:893–904.

37. Menkes HA, Traystman RJ. Collateral venti-lation. Am Rev Respir Dis. 1977;116:287–309.

38. Calzia E, Radermacher P. Airway pressure re-lease ventilation and biphasic positive airwaypressure: a 10-year literature review. ClinicalIntensive Care. 1997;8:296–301.

39. Falkenhain SK, Reilley TE, Gregory JS. Im-provement in cardiac output during airwaypressure release ventilation. Crit Care Med.1992;20:1358–1360.

40. Rasanen J, Downs JB, Stock MC. Cardiovascu-lar effects of conventional positive pressureventilation and airway pressure release venti-lation. Chest. 1988;3:911–915.

41. Froese AB, Bryan AC. Effects of anesthesiaand paralysis on diaphragmatic mechanics inman. Anesthesiology. 1974;41:242–255.

42. Putensen C, Rasanen J, Lopez FA. Ventilation-perfusion distributions during mechanicalventilation with superimposed spontaneousbreathing in canine lung injury. Am J RespirCrit Care Med. 1994;150:101–108.

43. Putensen C, Norbert JM, Putensen-Himmer G,Zinserling J. Spontaneous breathing duringventilatory support improves ventilation-per-fusion distributions in patients with acute res-piratory distress syndrome. Am J Respir CritCare Med. 1999;159:1241–1248.

44. Habashi NM. APRV: Principles and Practice.Luebeck, Germany: Draegerwerk. In press.

45. Martin LD, Wetzel RC. Optimal release timeduring airway pressure release ventilation inneonatal sheep. Crit Care Med. 1994;22:486–493.

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