Other approaches to open-lung ventilation: Airway pressure releaseventilationNader M. Habashi, MD, FACP, FCCP    Objective...
Conversely, spontaneous breathing favors                                                                                  ...
Table 1. Clinical studies using airway pressure-release ventilation (APRV)     Author (yr Published)                    St...
Because patients can maintain their                                                                                       ...
Figure 4. End-expiratory lung volume. Expiratory flow pattern during the release phase of airway pressure release ventilati...
Table 2. Airway pressure release ventilation (APRV) clinical guideGoals  Acute (recruitable) restrictive lung disease (RLD...
Table 2. ContinuedOxygenation  Optimize end-expiratory or release lung volume     Reassess release volume to ensure T-PEFR...
Figure 7. Gas flow pattern comparing pressure                                                                              ...
duration of mechanical ventilation de-         assist technique (119). The STC has            have similar goals. Both tec...
Figure 8. Airway pressure release ventilation weaning and gradual transition to pure continuous positive airway pressure (...
10. Varpula T, Jousela I, Niemi R, et al: Com-              ing; June 27–28, 2004; University of War-             Influence...
breath holding and rebreathing. J Appl                 and intrinsic positive end-expiratory pres-           Regional effe...
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APRV Review

  1. 1. Other approaches to open-lung ventilation: Airway pressure releaseventilationNader M. Habashi, MD, FACP, FCCP Objective: To review the use of airway pressure release ven- Conclusion: APRV may offer potential clinical advantages fortilation (APRV) in the treatment of acute lung injury/acute respi- ventilator management of acute lung injury/acute respiratoryratory distress syndrome. distress syndrome and may be considered as an alternative Data Source: Published animal studies, human studies, and “open lung approach” to mechanical ventilation. Whetherreview articles of APRV. APRV reduces mortality or increases ventilator-free days com- Data Summary: APRV has been successfully used in neonatal, pared with a conventional volume-cycled “lung protective”pediatric, and adult forms of respiratory failure. Experimental and strategy will require future randomized, controlled trials. (Critclinical use of APRV has been shown to facilitate spontaneous Care Med 2005; 33[Suppl.]:S228 –S240)breathing and is associated with decreased peak airway pres- KEY WORDS: airway pressure release ventilation; airway pres-sures and improved oxygenation/ventilation when compared with sure release ventilation; spontaneous breathing; lung protectiveconventional ventilation. Additionally, improvements in hemody- strategies; acute lung injury; acute respiratory distress syndromenamic parameters, splanchnic perfusion, and reduced sedation/neuromuscular blocker requirements have been reported.A irway pressure release ventila- flow follow a similar time course (7–9). by releasing airway pressure to a lower tion (APRV) was initially de- As a result, by allowing patients to spon- CPAP level termed Plow. The intermittent scribed by Stock and Downs (1, taneously breathe during APRV, depen- release in airway pressure during APRV 2) as continuous positive air- dent lung regions may be preferentially provides CO2 removal and partially un-way pressure (CPAP) with an intermittent recruited without the need to raise ap- loads the metabolic burden of pure CPAPpressure release phase. Conceptually, plied airway pressure. breathing.APRV applies a continuous airway pres- APRV has been used in neonatal, pe- By using a release phase for ventila-sure (Phigh) identical to CPAP to maintain diatric, and adult forms of respiratory tion, APRV uncouples the traditional re-adequate lung volume and promote alve- failure (1– 4, 6, 10 –22). Clinical studies quirement of elevating airway pressure,olar recruitment. However, APRV adds a using APRV are summarized in Table 1 lung volume, and distension during tidaltime-cycled release phase to a lower set (1– 4, 12, 18, 23–28). ventilation. Rather than generating apressure (Plow). In addition, spontaneous In patients with decreased functional tidal volume by raising airway pressurebreathing can be integrated and is inde- residual capacity (FRC), elastic work of above the set positive end-expiratorypendent of the ventilator cycle (Fig. 1). breathing (WOB) is effectively reduced pressure (PEEP) (like in conventionalCPAP breathing mimics the gas distribu- with the application of CPAP. As FRC is ventilation), release volumes in APRV aretion of spontaneous breaths as opposed to restored, inspiration begins from a more generated by briefly releasing airwaymechanically controlled, assisted, or sup- favorable pressure/volume relationship, pressure from Phigh to Plow. Because ven-ported breaths, which produce less phys- facilitating spontaneous ventilation and tilation with APRV results as airway pres-iological distribution (3– 6). Mechanical improving oxygenation (29). sure and lung volume decrease (releasebreaths shift ventilation to nondependent However, in acute lung injury/acute volume), the risk of overdistension maylung regions as the passive respiratory respiratory distress syndrome (ALI/ be reduced. In contrast, conventionalsystem accommodates the displacement ARDS), the surface area available for gas ventilation raises airway pressure, elevat-of gas in to the lungs. However, sponta- exchange is significantly reduced. Despite ing lung volumes, potentially increasingneous breathing during APRV results in a optimal lung volume, CPAP mandates the threat of overdistension (Fig. 2).more dependent gas distribution when that unaided spontaneous breathing Ventilation generated by the releasethe active respiratory system draws gas manage the entire metabolic load or CO2 phase of APRV may have additional ad-into the lung as pressure changes and production. However, CPAP alone may be vantages in ALI/ARDS. Increased elastic inadequate to accomplish necessary CO2 recoil is common to restrictive lung dis- From the Multi-trauma ICU, R Adams Cowley removal without producing excessive eases such as ALI/ARDS. With APRV, asShock Trauma Center, Baltimore, MD. WOB. In contrast to CPAP, APRV inter- airway pressure is briefly interrupted, the Copyright © 2005 by the Society of Critical Care rupts airway pressure briefly to supple- release volume is driven by gas compres-Medicine and Lippincott Williams & Wilkins ment spontaneous minute ventilation. sion and lung recoil (potential energy) DOI: 10.1097/01.CCM.0000155920.11893.37 During APRV, ventilation is augmented stored during the Phigh time period orS228 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)
  2. 2. Conversely, spontaneous breathing favors dependent lung recruitment through the application of pleural pressure. Sponta- neous breaths at the CPAP level (Phigh) improve dependent ventilation through pleural pressure changes rather than the application of additional applied airway pressure (5, 6, 26). The recruited lung requires less pressure than the recruiting lung. Therefore, maintaining lung vol- ume and allowing spontaneous breathing from the time of intubation by using APRV (CPAP with release) may reduce the need for recurrent high CPAP recruit- ment maneuvers (41). If a recruitment maneuver is desired during APRV, the Phigh and Thigh can be adjusted to simu- late a conventional CPAP-type recruit-Figure 1. Airway pressure release ventilation is a form of continuous positive airway pressure (CPAP). ment maneuver (e.g., Phigh 40 –50 cmThe Phigh is equivalent to a CPAP level; Thigh is the duration of Phigh. The CPAP phase (Phigh) is H2O and Thigh 30 – 60 secs).intermittently released to a Plow for a brief duration (Tlow) reestablishing the CPAP level on the Conventional volume ventilation lim-subsequent breath. Spontaneous breathing may be superimposed at both pressure levels and is its recruitment to brief cyclic intervals atindependent of time-cycling. Reprinted from ICON educational supplement 2004 with permission. end-inspiration or plateau pressure. Lung regions that are recruited only during brief end-inspiratory pressure cycles pro-Thigh. During conventional ventilation, spontaneous breaths at a high lung vol- duce inadequate mean alveolar volume.inspiratory tidal volumes must overcome ume rather than brief and frequent tidal Because alveolar volume is not main-airway impedance and elastic forces of ventilation between PEEP and end- tained, compliance does not improve, re-the restricted lung from a lower baseline inspiratory pressure may be more suc- quiring the same inflation pressure onresting volume, increasing the energy or cessful in achieving progressive and sus- subsequent breaths. Reapplication of thepressure required to distend the lung and tained alveolar recruitment. same distending pressure without ade-chest wall. Furthermore, as thoracic Airway opening is dynamic as the lung quate lung recruitment is likely to pro-compliance decreases, the inspiratory creeps to the recruited lung volume. duce recurrent shear forces and does notlimb of the volume/pressure curve shifts Compliance and resistance (time con- attenuate potential lung injury (42). Con-to the right, i.e., more pressure is re- stants) of recently recruited lung unitsquired to deliver a set tidal volume. How- decrease the inflating or sustaining pres- versely, sustained recruitment is associ-ever, the expiratory limb remains unaf- sure requirements. Therefore, progres- ated with increased compliance allowingfected by the prevailing volume/pressure sive extensions of Thigh may be critical for successful, sequential airway pressure re-relationship and extends throughout all sustaining recruitment as time constants duction and improving gas exchange byphases of injury (30). APRV uses the more evolve (38). Furthermore, the sustained increasing alveolar surface area (4, 42–favorable volume/pressure relationship of Thigh period may encourage spontaneous 44). Increased alveolar surface area maythe expiratory limb for ventilation by ap- breathing at an upper and open lung vol- improve stress distribution in the lung.plying a near-sustained inflation or re- ume, improving efficiency of ventilation. Gallagher and coworkers (45) demon-cruitment state (31). Although recruitment maneuvers may strated a direct correlation among mean Alveolar recruitment is a pan-inspira- be effective in improving gas exchange airway pressure, lung volume, and oxy-tory phenomenon. Successful recruiting and compliance, these effects appear to genation. The use of APRV to optimizepressure depends on the yield or thresh- be nonsustained, requiring repeated ma- mean airway pressure/lung volume pro-old opening pressure (TOP) of lung units. neuvers (39, 40). Alternatively, APRV may vides a greater surface area for gas ex-ALI/ARDS may have a multitude of TOP be viewed as a nearly continuous recruit- change. Allowing sustained durationdistributed throughout the lung (32–35). ment maneuver with the Phigh providing (Thigh) of Phigh and limiting duration andIn addition to TOP, the time-dependent 80% to 95% of the cycle time creating a frequency of the release phase (Tlow) ofnature of recruitment should also be con- stabilized “open lung” while facilitating Plow permits only partial emptying, lim-sidered. Although the exact mechanisms spontaneous breathing. Fundamentally, iting lung volume loss during ventilation.are not known, the lung is interdepen- assisted mechanical breaths cannot pro- As lung recruitment is sustained, gas re-dent and recruitment of air spaces results vide the same gas distribution as sponta- distribution and diffusion along concen-in radial traction of neighboring alveoli, neous breaths. Therefore, during a re- tration gradients have time to occur. Theproducing a time-dependent ripple effect cruitment maneuver in a passive mixture of alveolar and inspired gasof recruitment (36 –38). respiratory system, the nondependent within the anatomic dead space results in As lung units recruit, the additional lung regions distend first until applied a greater equilibration of gas concentra-time (Thigh) at Phigh provides stability as airway pressure reaches and exceeds the tions in all lung regions, improved oxy-an “avalanche” of lung units pop open high TOP of the dependent lung units, genation, and reduced dead-space venti-(37, 38). Conceptually, superimposed increasing the threat of overdistention. lation (26, 46) (Fig. 3).Crit Care Med 2005 Vol. 33, No. 3 (Suppl.) S229
  3. 3. Table 1. Clinical studies using airway pressure-release ventilation (APRV) Author (yr Published) Study Measurements Findings Study designStock (1987) APRV vs. IPPV; dogs with ALI Blood gases, hemodynamics, Hemodynamics were not Animal study, small n, and (n 10) lung volume, airway different at equivalent VE; with short-term observations pressure, f, VT, VE APRV, PIP and physiological dead space were lower, mean airway pressure was higher, and oxygenation was betterGarner (1988) APRV vs. conventional ventilation, Blood gases, hemodynamics, Similar oxygenation and Observational, crossover patients after cardiac surgery lung volume, airway ventilation at lower peak trial (n 14) pressure, f, VT, VE airway pressureRasanen (1988) APRV vs. conventional ventilation Blood gases, hemodynamics, APRV had similar effects on Animal studies, small n, vs. CPAP; anesthetized dogs lung volume, airway blood gases but with and short-term (n 10) pressure, f, VT, VE significantly fewer adverse observations hemodynamic effectsMartin (1991) APRV vs. CPAP vs. conventional Blood gases, hemodynamics, APRV increased VE more than Animal studies, small n, ventilation vs. spontaneous lung volume, airway CPAP; APRV provided similar and short-term breathing; neonatal sheep with pressure, f, VT, VE gas exchange to conventional observations oleic-acid lung injury (n 7) ventilation, but with fewer adverse hemodynamic effectsDavis (1993) APRV vs. SIMV; surgery patients Blood gases, hemodynamics, APRV provided similar gas Prospective, crossover trial with ALI lung volume, airway exchange with lower PIP, but with short-term (n 15) pressure, f, VT, VE no hemodynamic advantage observations was identifiedPutensen (1994) APRV (with and without Blood gases, hemodynamics, PSV had highest VE; APRV had Animal studies, small n, spontaneous breathing) vs. lung volume, airway higher cardiac output, PaO2, and short-term PSV; anesthetized dogs pressure, f, VT, VE, and oxygen delivery; APRV had observations (n 10) ventilation/perfusion better V/Q and less dead space determined by multiple inert-gas-elimination techniqueSydow (1994) APRV vs. volume-controlled Blood gases, hemodynamics, APRV provided 30% lower PIP, Prospective, randomized, inverse-ratio ventilation; lung volume, airway less venous admixture (14 vs. crossover trial patients with ALI; 24-hr pressure, f, VT, VE 21%), and better oxygenation; observation periods (n 18) no difference in hemodynamicsCalzia (1994) BiPAP vs. CPAP; patients after WOB and PTP No difference Prospective, crossover trial bypass surgery (n 19)Rathgeber (1997) BiPAP vs. conventional ventilation Duration of intubation, APRV had shorter duration of Prospective, randomized, vs. SIMV; patients after cardiac sedation requirement, intubation (10 hrs) than SIMV controlled, open trial surgery (n 596) analgesia requirement (15 hrs) or conventional over 18 months, uneven ventilation (13 hrs); randomization conventional ventilation was associated with greater doses of midazolam; APRV was associated with less need for analgesiaKazmaier (2000) BiPAP vs. SIMV vs. PSV; pPatients Blood gases, hemodynamics, No differences in blood gases or Prospective, crossover trial after coronary artery bypass lung volume, airway hemodynamics with short-term (n 24) pressure, f, VT, VE observationsPutensen (2001) APRV vs. pressure controlled Gas exchange, APRV was associated with fewer Randomized controlled, conventional ventilation; hemodynamics, sedation ICU days, fewer ventilator prospective trial, small patients with ALI after trauma requirement, days, better gas exchange, n; the conventional (n 30) hemodynamic support, better hemodynamic ventilation group duration of ventilation, performance, better lung received paralysis for the ICU stay compliance, and less need for first 3 days, potentially sedation and vasopressors confounding resultsVarpula (2003) Combined effects of proning and Blood gases, oxygenation Oxygenation was significantly Prospective, randomized SIMV PC/PS vs. APRV; patients (PaO2/FIO2 ratio), better in APRV group before intervention study with ALI (n 45) hemodynamic, sedation and after proning; sedation use requirement and hemodynamics were similar IPPV, intermittent positive-pressure ventilation; ALI, acute lung injury; f, respiratory frequency; VE, minute volume; VT, tidal volume; PIP, peakinspiratory pressure; CPAP, continuous positive airway pressure; PSV, pressure support ventilation; V/Q, ventilation/perfusion ratio; BiPAP, bilevel positiveairway pressure; SIMV, synchronized intermittent mandatory ventilation; WOB, work of breathing; PTP, pressure-time product; ICU, intensive care unit. Reprinted with permission from Branson RD, Johannigman JA: What is the evidence base for the newer ventilation modes? Respir Care 2004;49:742–760. In addition to FIO2 and slope, clini- The Phigh and Thigh regulate end- face area of open air spaces for diffusivecian-controlled APRV parameters are: inspiratory lung volume and provide a gas movement. As a result, these param-Phigh, Thigh, Plow, and Tlow. Time parame- significant contribution to the mean air- eters control oxygenation and alveolarters in APRV are independent rather than way pressure. Mean airway pressure cor- ventilation. Counterintuitive to conven-an inspiratory:expiratory (I:E) ratio al- relates to mean alveolar volume and is tional concepts of ventilation, the exten-lowing precise adjustment. critical for maintaining an increased sur- sion of Thigh can be associated with aS230 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)
  4. 4. Because patients can maintain their native respiratory drive during APRV, spontaneous inspiratory and expiratory time intervals are independent of the Thigh, Tlow cycle (56). Thus, the release phase does not reflect the only expiratory time during APRV when patients areFigure 2. Ventilation during airway pressure release ventilation is augmented by release volumes and breathing spontaneously. Therefore,is associated with decreasing airway pressure and lung distension. Conversely, tidal volumes during spontaneous expirations will occur at theconventional ventilation are generated by increasing airway pressure and lung distension. Reprintedfrom ICON educational supplement 2004 with permission. upper pressure or Phigh phase. Active ex- halation during the Phigh phase may re- sult in additional recruitment and vol- ume redistribution analogous to grunting respiration in neonates, thereby improving ventilation/perfusion (V/Q) matching (22, 57– 61). The release time (Tlow) may be titrated to maintain end-expiratory lung volume (EELV)/(end-release lung volume [ERLV]). The end-release lung volume can be ad- justed and continually assessed by using the expiratory flow pattern (Fig. 4). The expiratory gas flow is a result of the inspira- tory lung volume, the recoil or drive pres- sure of the lung, and downstream resis- tance (artificial airway, circuit, and PEEP valve) (Fig. 5). Experimental data in a por- cine ALI model using dynamic computed tomography scanning shows that airwayFigure 3. Gas exchange during airway pressure release ventilation. A, mean airway pressure (lung closure occurs rapidly (within 0.6 secs) (38,volume) provides sustained mean alveolar volume for gas diffusion. B, alveolar gas volume combinedwith cardiac output provides continuous diffusive gas exchange between alveolar and blood compart- 62). However, the rapid airway closure inments despite the cyclic nature of ventilation. C, CO2-enriched gas is released to accommodate pig models of ALI may be related to pooroxygen-enriched gas delivered with the subsequent inspiratory cycle. New inspiratory volume is collateral ventilation as opposed to humanintroduced, regenerating diffusion gradients. Reprinted from ICON educational supplement 2004 with lungs. Collateral ventilation may play a sig-permission. nificant role in recruitment/derecruitment in ALI (63). Using a P low of zero allows end-decrease in PaCO2 as machine frequency Thigh will lead to a reduction in mean expiratory/release lung volume to be con-decreases. This has been previously de- airway pressure, potentially resulting in trolled by one parameter (time). The in-scribed and is similar to improved CO2 airway closure, decreasing alveolar sur- herent resistance of the artificial airwayclearance with increasing I:E ratios (47– face area for gas exchange. behaves as a flow resistor/limiter and, if51). Despite the intermittent nature of In addition to spontaneous breathing, coupled with a brief release time, canventilation, CO2 delivery to the lung is ventilation is augmented during APRV as effectively trap gas volume to maintaincontinuous as cardiac output transfers a result of the release phase. The release end-release or expiratory pressureCO2 into the alveolar space, provided air- phase is determined by the driving pres- (PEEP) (64, 65). During passive expira-ways remain open (52). During the brief sure differential (Phigh - Plow), inspiratory tion or release in patients with ARDS,Tlow, released gas is exchanged with fresh lung volume (Phigh), the potential energy expiratory time constants are signifi-gas to regenerate the gradient for CO2 cantly modified (increased threefold) by (recoil or compliance of the thorax anddiffusion. In addition, cardiogenic mixing the flow-dependent resistance of the arti- the amount of energy stored duringresults in CO2 movement toward central ficial airway (66, 67). Thigh), and downstream resistance (artifi-airways during the Thigh or breathhold Because the artificial airway produces a cial airway). Plow and Tlow regulate end-period (46, 53–55), improving the efficacy nonlinear, flow-dependent resistive loadof the release for ventilation. The addi- expiratory lung volume and should be and the release results from a high lungtion of spontaneous breaths during the optimized to reduce airway closure/ volume, flow resistance will be highest atThigh period at Phigh (higher lung volume) derecruitment and not as a primary ven- the initial portion of the release phase (67–further enhances recruitment and venti- tilation adjustment. Generally, to main- 69). The Tlow or release phase is terminatedlation efficiency (Fig. 3). tain maximal recruitment, the majority T-PEFR rapidly before the flow-dependent The risk of using APRV as a cyclic of the time or Thigh (80 –95% of the total expiratory load is dissipated, resulting inmode and attempting to increase the ma- cycle time) occurs at the Phigh or CPAP end-expiratory volume and pressure.chine frequency and minute ventilation level. To minimize derecruitment, the The residual pressure and volume inby reducing Thigh may sacrifice alveolar time (Tlow) at Plow is brief (usually be- the lung during the brief release phaseventilation and oxygenation. Reducing tween 0.2 and 0.8 secs in adults). typically yields end-release or end-Crit Care Med 2005 Vol. 33, No. 3 (Suppl.) S231
  5. 5. Figure 4. End-expiratory lung volume. Expiratory flow pattern during the release phase of airway pressure release ventilation. Initial portion of expiratoryflow limb is the peak expiratory flow rate (PEFR) as a result of Phigh to Plow pressure reduction. Deceleration of gas flow occurs as driving pressure dissipatesproducing the decelerating limb. PEFR and rate of deceleration are affected by inspiratory lung volume, thoracic recoil, and downstream resistance(artificial airway resistance with Plow of zero). A, expiratory flow pattern demonstrating normal deceleration at 45° as airways empty sequentially (67).Release time is adjusted to regulate T-PEFR to 60% of PEFR. The flow/time beyond the T-PEFR correlates with the end-release lung volume (ERLV)(end-expiratory lung volume [EELV]). The angle of deceleration (ADEC) can suggest alterations in lung mechanics resulting in altered expiratory gas flow([a] Normal (45°), [b] restrictive, e.g., decrease thoracic compliance ( 45°) [c] obstructive, e.g., OLD, small or obstructed artificial airway ( 45°)]. B,expiratory flow pattern with lung changes indicating derecruitment. As lung compliance worsens (less end-inspiratory lung volume and increasing thoracicrecoil, e.g., increased lung water or decreased thoracic/abdominal compliance), the expiratory flow pattern will become more restricted (the deceleratinglimb will become steeper, i.e., ADEC 45°) and the set release time will result in a lower T-PEFR and less end-expiratory lung volume (or ERLV); lowerERLV with resulting airway closure/derecruitment. C, the release time can be adjusted to limit airway closure and prevent derecruitment. D, conversely,as respiratory mechanics improve (lung, thoracic, abdominal compliance), recruitment is reflected as the decelerating limb returns to a 45° angle and theset release time increases the T-PEFR regulating ERLV (EELV). E, the release time can be readjusted to maintain T-PEFR at 50% to 75%. Reprinted fromICON educational supplement 2004 with permission. to subatmospheric is required to fully compensate the expiratory resistance im- posed by the artificial airway (70). By using a Plow 0 cm H2O, peak expi- ratory flow rate (PEFR) is delayed, whereas a Plow of 0 cm H2O accelerates PEFR con- cluding the release phase earlier and en- abling the Phigh phase to be resumed earlier in the cycle. A greater percent of the cycle time at Thigh increases the potential for recruitment, maintains lung volume, limits derecruitment, and induces spontaneous breathing. See Table 2 for goals, set up,Figure 5. Patient interface to mechanical ventilator circuit and inherent resistance to expiratory flow oxygenation, ventilation, weaning, and pre-from artificial airway (R1) and positive end-expiratory pressure (PEEP) valve (R2). Because the release cautions during utilization of APRV.occurs from a high lung volume during airway pressure release ventilation, flow resistance developsat the distal end of R1 and R2. The proximal end of R1 decompresses more rapidly than the distal end. Spontaneous Breathing DuringDespite zero end-expiratory pressure (ZEEP), flow resistance at R2 (typically measured approximately Airway Pressure Release8 ft away) contributes to tracheal pressure elevation above end-expiratory pressure. Flow resistance ishighest at the onset of the release ( 0.2 L/sec) and decreases as expiratory flow rate declines. Release Ventilationtime is terminated after a brief duration before flow resistance dissipates to maintain end-expiratory During APRV, patients can control thelung volume (67– 69). Reprinted from ICON educational supplement 2004 with permission. frequency and duration of spontaneous inspiration and expiration. Patients areexpiratory pressure greater than the Plow of artificial airways provide inadequate not confined to a preset I:E ratio, andarbitrarily set at the machine’s peep valve expiratory compensation when PEEP is spontaneous tidal volumes maintain a si-(approximately 8 ft away). In fact, com- reduced to atmospheric pressure. The ad- nusoidal flow pattern similar to normalmercially available ventilators with tube dition of a negative pressure source to spontaneous breaths. The ability of criti-compensation algorithms for resistance briefly lower the end-expiratory pressure cally ill patients to effectively augmentS232 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)
  6. 6. Table 2. Airway pressure release ventilation (APRV) clinical guideGoals Acute (recruitable) restrictive lung disease (RLD) Increase (recruit) and maintain lung volume (Phigh and Thigh) Decrease elastic WOB with CPAP (Phigh and Thigh) ATC set at 100% to maximally compensate for artificial airway resistance and decrease resistive WOB imposed by the artificial airwaya Minimize number of releases to supplement ventilation from spontaneous breathing (71) Limit derecruitment; Tlow set to ensure T-PEFR is 50 and 75% Allow spontaneous breathing within 24 hrs of APRV application Acute obstructive lung disease (OLD) Decrease lung volume Maintain Phigh at or 1–2 cm H2O above PEEPi Minimize number of releases to supplement ventilation from spontaneous breathing (71) Stint airways; Tlow set for 25–50% T-PEFR Allow spontaneous breathing within 24 hrs of APRV application. May require a brief course of NMBA ( 24 hrs) to control high spontaneous breathing frequency and artificial airway contribution to dynamic hyperinflation.Set-up—adults Newly intubated Phigh—set at desired plateau pressure (typically 20–35 cm H2O) Note: Phigh 35 cm H2O may be necessary in patients with decreased thoracic/abdominal compliance or morbid obesity (73, 74). With a Phigh 25 cm H2O, use of noncompliant ventilator circuit is recommended to minimize circuit volume compression (75, 76). Plow—0 cm H2O Thigh—4–6 secs Tlow—0.2–0.8 secs (RLD) 0.8–1.5 secs (OLD) Transition from conventional ventilation Phigh—plateau pressure in volume-cycled mode or peak airway pressure in pressure-cycled mode Plow—0 cm H2O Thigh—4–6 secs Tlow—0.2–0.8 secs (RLD) 0.8–1.5 secs (OLD) Transition from HFOVb—use noncompliant ventilator circuit Phigh—mPaw on HFOV plus 2–4 cm H2O Plow—0 cm H2O Thigh—4–6 secs Tlow—0.2–0.8 secs (RLD) 0.8–1.5 secs (OLD)Set-up—Pediatrics Newly intubated Phigh—set at desired plateau pressure (typically 20–30 cm H2O) Note: Phigh 30 cm H2O may be necessary in patients with decreased thoracic/abdominal compliance or morbid obesity (73, 74). With a Phigh 25 cm H2O, use of noncompliant ventilator circuit is recommended to minimize circuit volume compression (75, 76). Plow—0 cm H2O Thigh—3–5 secs Tlow—0.2–0.8 Transition from conventional ventilation Phigh—plateau pressure in volume-cycled mode or peak airway pressure in pressure-cycled mode Plow—0 cm H2O Thigh—3–5 secs Tlow—0.2–0.8 Transition from HFOVb Phigh—mPaw on HFOV plus 2–4 cm H2O Plow—0 cm H2O Thigh—3–5 secs Tlow—0.2–0.8Set-up—Neonates Newly intubated Phigh—set at desired plateau pressure (typically 10–25 cm H2O) Note: Phigh 25 cm H2O may be necessary in patients with decreased thoracic/abdominal compliance (73, 74). With a Phigh 25 cm H2O, use of noncompliant ventilator circuit is recommended to minimize circuit volume compression (75, 76). Plow—0 cm H2O Thigh—2–3 secs Tlow—0.2–0.4 Transition from conventional ventilation Phigh—plateau pressure in volume-cycled mode or peak airway pressure in pressure-cycled mode Plow—0 cm H2O Thigh—2–3 secs Tlow—0.2–0.4 Transition from HFOVb Phigh—mPaw on HFOV plus 0–2 cm H2O Plow—0 cm H2O Thigh—2–3 secs Tlow—0.2–0.4 ContinuesCrit Care Med 2005 Vol. 33, No. 3 (Suppl.) S233
  7. 7. Table 2. ContinuedOxygenation Optimize end-expiratory or release lung volume Reassess release volume to ensure T-PEFR is 50 and 75% If oxygenation poor and T-PEFR 50%, decrease release time until T-PEFR 75% Optimize gas exchange surface area by adjusting mPaw Increase Phigh or Phigh and Thigh simultaneously Adjustment of Phigh to recruit by achieving TOP Adjustment of Thigh increases gas mixing and recruits lung units with high resistance time constants Assess hemodynamicsVentilation Assess for oversedation; consider using sedation scale (77) Optimize end-expiratory or release lung volume; reassess release volume to ensure at 50–75% T-PEFR If T-PEFR 75% and oxygenation is acceptable, consider increasing Tlow by 0.05–0.1 increments to achieve 50% T-PEFR If T-PEFR 50%, decrease Tlow to achieve minimum T-PEFR of 50% Increase alveolar ventilation (preferred method)—increase Phigh or Phigh and Thigh simultaneously Increase minute ventilation—decrease Thigh and increase Phigh simultaneously (see precautions below)Weaning Simultaneously reduce Phigh and increase Thigh for a gradual reduction of mPaw and to increase the contribution of spontaneous to total minute ventilation. Progress to CPAP with automatic tube compensation when Phigh 16 and Thigh 12–15 sec (APRV 90% CPAP) Wean CPAP (with automatic tube compensation) and consider extubation when CPAP 5–10 cm H2OPrecautions Adjustment of Tlow differs with lung disease, lung volume and artificial airway size. Tlow values provided are typical but not absolute; see goals for OLD and RLD If minute ventilation is increased by decreasing Thigh in an attempt to improve CO2 clearance, mPaw and gas exchanging surface area will be reduced; more so if Phigh is not simultaneously increased as CO2 may paradoxically increase (see text for details). May need to decrease Tlow as Thigh reduction may produce less mean alveolar volume (lung volume) and will result in shorter emptying time. Tlow should not be extended solely to lower CO2 as this may lead to airway closure (derecruitment) (38, 56, 71). Additionally, Tlow should not be viewed as an expiratory time as the patient may exhale throughout the respiratory cycle if permitted (58). ATC, automatic tube compensation; PEEPi, intrinsic PEEP; mPaw, mean airway pressure; PEFR, peak expiratory flow rate; T-PEFR, peak expiratory flowrate termination; HFOV, high-frequency oscillatory ventilation; WOB, work of breathing; APRV, airway pressure release ventilation; TOP, threshold openingpressure. a In vitro resistance may be greater than in vivo resistance calculations and measurements (commercial tube compensation algorithms) due todeformation, kinks and secretion in the artificial airway (64, 65, 72); bmPaw during HFOV is equal to CPAP; mPaw during APRV is typically 2– 4 cm H2Oless than CPAP as a result of the release phase (airway pressure interruption) and proximal vs. distal mPaw measurement. Reprinted from ICON EducationalSupplement—2004 with permission.spontaneous ventilation in response to pleural pressure, improving transalveolar mean systemic pressure (MSP)/RA gradientchanging metabolic needs may promote pressure gradients in dependent lung re- couples the thoracic and cardiac pumps,synchrony during mechanical ventilation gions (7, 84 – 87). Increased dependent increasing venous return, improving car-and improve V/Q matching (3– 6, 10, 11). lung ventilation during spontaneous diac output, and decreasing dead space ven-In contrast, patients transitioned from breathing recruits alveoli improving V/Q tilation (88, 89). Conversely, when sponta-spontaneous breathing to mechanical matching without raising applied airway neous breathing is limited or theventilation through the induction of an- pressure (3– 6, 10, 11). diaphragm is paralyzed, the passive decentesthesia exhibit worsening gas exchange APRV and prone positioning may of the diaphragm is no longer linked withand dependent atelectasis on computed have an additive effect on recruitment lower pleural/right atrial pressure, mini-tomography scan within minutes (7–9, and gas exchange. Varpula demon- mizing the IVC–right atrial pressure gradi-76 – 83). These studies suggest rapid al- strated greater improvement in gas ex- ent (MSP-RA) and limiting venous return/teration of ventilation distribution when change when prone positioning was cardiac output.the respiratory system becomes passive. combined with APRV rather than syn- Restoration of cardiopulmonary inter- Most mechanical ventilators monitor chronized intermittent mandatory ven- action with spontaneous breathing dur-airway pressures; however, transpulmo- tilation (10). ing APRV produces improvements in sys-nary pressures ultimately determine lung temic perfusion. Animal and humanvolume change. Although difficult to Hemodynamic Effects of Airway studies document improved splanchnicmonitor clinically, the effects of pleural Pressure Release Ventilation and renal perfusion during APRV withpressure on transpulmonary pressures spontaneous breathing (13, 90)should not be excluded from manage- The descent of the diaphragm into thement principles. For example, patients abdomen during a spontaneous breathing Use of Pressure Supportwith reduced thoracic and abdominal effort simultaneously decreases pleural Ventilation with Airway Pressurecompliance demonstrate higher airway pressures and increases abdominal pres- Release Ventilationpressure yet may have lower transpulmo- sure. This effectively lowers the right atrialnary pressure (73, 74). (RA) pressure while compressing abdomi- Currently, some ventilator manufac- Spontaneous breathing, diaphrag- nal viscera propelling blood (preload) into turers incorporate pressure support ven-matic tone, and prone positioning modify the inferior vena cava (IVC). Increasing the tilation (PSV) above Phigh. The addition ofS234 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)
  8. 8. Figure 7. Gas flow pattern comparing pressure support ventilation (PSV) and spontaneous breathing. PSV produces a decelerating gas flow pattern because the gas flow and patient effort (P Mus) do not follow a similar time course. Typi- cally, patient effort is outpaced by applied flow and pressure development. Gas distribution dur- ing PSV is similar to an assisted breath rather than a spontaneous breath. Spontaneous or un- assisted continuous positive airway pressure (CPAP) breath producing a sinusoidal gas flowFigure 6. A, pressure tracing represents a pressure support ventilation (PSV) breath at the Phigh level. pattern as gas flow and patient effort (P Mus) areDuring passive efforts, once the PSV trigger threshold is reached, airway pressure elevates above the coupled and follow a similar time course. Sponta-Phigh level. Alternatively, if the patient generates vigorous inspiratory efforts, the transpulmonary pressure neous ventilation (unassisted) is associated withdifferential (sum of PSV, Phigh, Pmus) can be significant and may result in overdistension. B, flow tracing improved ventilation/perfusion distribution, unlikedemonstrates a triggered PSV breath with resultant decelerating gas flow as opposed to sinusoidal gas flow PSV (4, 6, 26, 92–94). Reprinted from ICON educa-typical of spontaneous breathing (see D). C, pressure tracing represents airway pressure release ventilation tional supplement 2004 with permission.(APRV) with automatic tube compensation; note minimal airway pressure elevation above Phigh. D,spontaneous breaths during APRV with automatic tube compensation, preserving a sinusoidal flow pattern.Reprinted from ICON educational supplement 2004 with permission. applying a fixed airway pressure like PSV may result in both over- and un-PSV to APRV contradicts limiting airway than spontaneous breaths, especially if dercompensation of artificial airway re-pressure and lung distension during ven- adequate PEEP levels are used (95, 96). sistance as patient effort (flow) varies.tilation by not restricting lung inflation If patient efforts are more vigorous, the Commercially available ventilators offerto the Phigh level. PSV will undercompensate artificial air- forms of tube compensation but vary in the PSV above Phigh may lead to signifi- way resistance. efficiency of the algorithms applied. Al-cant elevation in transpulmonary pres- though many ventilators may compensatesure (Fig. 6). When PSV is triggered Artificial Airway Compensation inspiratory resistance effectively, expiratoryduring the Phigh phase, the higher base- Algorithms and Airway Pressure compensation by lowering PEEP levels toline lung volume distends further as the atmosphere or ZEEP (at the initial phase of Release Ventilationsum of Phigh, PSV, and pleural pressure expiration) may not unload expiratory re-raises transpulmonary pressure. The Computerized ventilator algorithms, sistance imposed by the artificial airway.additional lung distension above Phigh which attempt to match inspiratory flow to The application of negative airway pressureand the transpulmonary pressure eleva- calculated resistance of the artificial airway during the initial expiration phase may betion will not be completely reflected in during APRV may reduce spontaneous necessary to negate the pressure dropthe airway pressure because the pleural WOB (14). Unlike PSV, tube compensation across the artificial airway (70).pressure remains unknown (91). Fur- algorithms apply inspiratory flow in pro-thermore, the imposition of PSV to portion to the pressure drop across the Airway Pressure ReleaseAPRV reduces the benefits of spontane- artificial airway resulting from patient Ventilation and Use of Sedationous breathing by altering sinusoidal effort or flow demands (95, 96). As a and Neuromuscular-Blockingspontaneous breaths to decelerating as- result, the dynamic pressure applied to Agentssisted mechanical breaths as flow and the artificial airway is determinedpressure development are uncoupled within the breath cycle, limiting over- Sedation is essential when caring forfrom patient effort (Fig. 7). Ultimately, or undercompensation of artificial air- critically ill and injured patients re-PSV during APRV defeats improvements way resistance. Furthermore, as tube quiring mechanical ventilation. In se-in distribution of ventilation and V/Q compensation is coupled to patient ef- vere cases of patient–ventilator dys-matching associated with unassisted fort, flow and resulting applied airway synchrony, neuromuscular-blockingspontaneous breathing (4, 6, 26, 92– pressure do not exceed inspiratory pres- agents (NMBAs) are frequently used.94). During weaning, even low levels of sure generated by the respiratory mus- Excessive sedation has been associatedPSV used to overcome tube resistance cles (Pmus) (patient’s effort), preserving with increased duration of mechanicalmay overcompensate and convert pa- the sinusoidal flow pattern of spontane- ventilation in patients with acute respi-tient-triggered efforts to assisted rather ous breathing (97) (Fig. 6). Conversely, ratory failure (98 –103). Reducing theCrit Care Med 2005 Vol. 33, No. 3 (Suppl.) S235
  9. 9. duration of mechanical ventilation de- assist technique (119). The STC has have similar goals. Both techniques focuscreases patient exposure to artificial logged over 50,000 patient-hours annu- on maintaining lung volume while limit-airways, sedation, and NMBAs and the ally on APRV since 1994, developing sig- ing the peak ventilating pressure. Main-likelihood of ventilator-associated nificant clinical experience with APRV. At taining lung volume optimizes V/Qpneumonia (VAP) (101, 104 –106). STC, the 2-yr period post-APRV imple- matching, improves gas exchange, and The negative impact of sedation and mentation for the management of ad- improves stress distribution, minimizingNMBAs on the duration of mechanical vanced respiratory failure was studied shear forces. During HFOV, the continu-ventilation and the risk of VAP is likely to and documented a reduction in ARDS ous, high-flow gas pattern facilitates abe in part related to depression of the mortality and multisystem organ failure. constant airway pressure profile mini-cough reflex, increasing the risk of aspi- The mortality rates after the implemen- mizing derecruitment. In contrast toration of pharyngeal secretions (107). tation of APRV in patients meeting crite- HFOV, APRV actively promotes spontane-Watando suggested that improved cough ria for ARDS were lower than reported in ous breathing.reflex may limit aspiration pneumonia in the ARDSNet trial, 21.4% vs. 31% (120). In addition, APRV does not require ahigh-risk groups (108). Furthermore, an In addition, sedation requirements were single-purpose ventilator, effectively useseffective cough may be a predictor of hos- reduced and NMBA use essentially elimi- conventional humidification systems,pital mortality and of successful extuba- nated from routine practice at STC. and is associated with reduced sedationtion (109). and NMBA use. Furthermore, because Because APRV uses an open breathing Weaning from Airway Pressure ALI can develop in 24% of patients receiv-system and requires less sedation, pa- Release Ventilation ing mechanical ventilation who did nottients can exhale or cough throughout have ALI at the onset (122), APRV as athe respiratory cycle. As a result, cough Patients with improved oxygenation lung protective strategy, may be used ear-and secretion clearance can be facilitated on APRV (e.g., FIO2 40% with SpO2 lier rather than at advanced stages ofwithout significant intrathoracic pres- 95%) can be progressively weaned by respiratory failure. APRV can be appliedsure elevation or airway pressure-limit- lowering the Phigh and extending the as the initial ventilator mode for respira-ing as would occur with a closed expira- Thigh. By decreasing the number of re- tory failure or typically before HFOV cri-tory valve system. leases, the minute ventilation output of teria are reached. For patients showing APRV has been associated with a 70% the ventilator is reduced while simulta- improvement on HFOV, APRV may rep-reduction in NMBA requirements and a neously (if permitted) the patient’s spon- resent an ideal transition/weaning modal-30% to 40% reduction in sedation re- taneous minute ventilation increases, ity because Phigh on APRV can be matchedquirements when compared with conven- enabling a progressive spontaneous to the mean airway pressure (mPaw) dur-tional ventilation (3, 4, 11, 12, 23, 25, breathing trial (99) (Fig. 8). The total and ing HFOV, permitting continued gradual110). In addition, some studies suggest a spontaneous minute ventilation should reduction of lung volume (123).decrease in ventilator days and intensive be carefully monitored during weaning tocare unit and hospital length of stay as a anticipate changes in PaCO2. Eventually,result of using APRV (4). the ventilator’s minute ventilation output Noninvasive Ventilation with The ARDS Network (ARDSNet) re- is significantly reduced or eliminated and Airway Pressure Releaseported a significant reduction of mortal- the patient has gradually transitioned to Ventilationity from 39.8% to 31.0% with a low tidal pure CPAP. CPAP, when combined withvolume strategy (6 mL/kg of ideal body tube compensation, can be used to effec- APRV may also be applied noninva-weight) and a limited inspiratory plateau tively overcome artificial airway resis- sively pre- or postintubation (124). Non-pressure (30 cm H2O) using a volume- tance during the final phase of weaning. invasive APRV has the advantage of ancycled mode (111). However, patients When used in the final weaning phase, adjustable degree of mandatory ventila-ventilated using low tidal volumes may tube compensation may be a useful pre- tion without the need for a trigger (onlyexperience more dyssynchrony and re- dictor of successful extubation, particu- forms of APRV that do not use pressurequire additional sedation (Kallet RH, per- larly in the difficult-to-wean patient who support), decreasing the likelihood of au-sonal communication) (112–118). fails PSV and T-piece weaning methods tocycling from leaks common to nonin- (96). This author believes that progres- vasive ventilation.Airway Pressure Release sive extension of Thigh during APRV wean- Future clinical research with APRVVentilation for Trauma- ing increases spontaneous breathing should test different algorithms for oxy-Associated Acute Respiratory through a gradual transition to pure genation, ventilation, and weaning. In ad-Distress Syndrome: Clinical CPAP (with tube compensation). There- dition, hemodynamic and systemic perfu- fore, transitioning the weaning APRV pa- sion during APRV should be assessed.Experience tient to PSV (a form of assisted breathing) Animal studies should be performed with APRV has been used at R Adams Cow- may be counterproductive and unneces- APRV (coupled with spontaneous breath-ley Shock Trauma Center (STC) in Balti- sary (121). ing) to compare histologic and biomarkermore, MD, since 1994 and has become a evidence of VILI/VALI compared withstandard of care. In the early 1990s, STC Airway Pressure Release other mechanical ventilation approaches.established a regional advanced respira- Ventilation and High-Frequency The delivery of aerosol medications to thetory failure service, including the devel- Oscillatory Ventilation lung is poorly understood during APRVopment of ventilation protocols aimed to and should be studied. Ultimately, clini-reduce airway pressure with APRV, prone Fundamentally APRV and high-fre- cal studies should be conducted using apositioning, and an extracorporeal lung quency oscillatory ventilation (HFOV) validated, protocolized approach to APRVS236 Crit Care Med 2005 Vol. 33, No. 3 (Suppl.)
  10. 10. Figure 8. Airway pressure release ventilation weaning and gradual transition to pure continuous positive airway pressure (CPAP). Tube compensation maybe used with the onset of spontaneous breathing and is not limited to the final weaning phase. A, sequentially decreasing Phigh and increasing Thighsimultaneously results in a gradual reduction of mean airway pressure. Mean airway pressure is reshaped to produce a lower and extended pressure profile.B, patient’s increased spontaneous minute ventilation increases as fewer releases in Phigh contribute less to the total minute ventilation. Eventually, therelease phase provides minimal contribution to the total minute ventilation, and the patient has transitioned to CPAP (tube compensate remains active).Reprinted from ICON educational supplement 2004 with permission.compared with a protective conventional lung” approaches to lung protective lease ventilation and volume-controlled in-ventilation strategy. mechanical ventilation with the ability verse ratio ventilation. Am J Respir Crit to facilitate spontaneous breathing. Care Med 1994; 149:1550 –1556 4. Putensen C, Zech S, Wrigge H, et al: Long-CONCLUSION term effects of spontaneous breathing dur- ACKNOWLEDGMENTS ing ventilatory support in patients with Clinical and experimental studieswith APRV demonstrate improvements We thank John Downs for review of acute lung injury. Am J Respir Crit Carein physiological end points such as gas Med 2001; 164:43– 49 the manuscript and Penny Andrews for 5. Wrigge H, Zinserling J, Neumann P, et al:exchange, cardiac output, and systemic review and assistance with the manu- Spontaneous breathing improves lung aer-blood flow (3, 4, 6, 11, 13, 26, 90). APRV script; Ulf Borg for review of the manu- ation in oleic acid-induced lung injury. An-facilitates spontaneous breathing and script; and Alastair A. Hutchison for ob- esthesiology 2003; 99:376 –384improves patient tolerance to mechan- servation and contribution on neonatal 6. Putensen C, Mutz N, Putensen-Himmer G,ical ventilation by decreasing patient– breathing pattern during airway pressure et al: Spontaneous breathing during venti-ventilator dyssynchrony. Additional release ventilation. latory support improves ventilation-perfu-studies document reduction in sedation sion distributions in patients with acute re-and NMBAs with APRV, and some, but REFERENCES spiratory distress syndrome. Am J Respirnot all (10), studies suggest less venti- Crit Care Med 1999; 159:1241–1248lator days and shorter length of inten- 1. Downs JB, Stock MC: Airway pressure re- 7. Froese A, Bryan C: Effects of anesthesia andsive care unit stay (3, 4, 11, 12, 23, 25, lease ventilation: a new concept in ventila- paralysis on diaphragmatic mechanics in tory support. Crit Care Med 1987; 15: man. Anesthesiology 1974; 41:242–255111). An adequately designed and pow- 459 – 461 8. Rehder K, Sessler AD: Regional intrapulmo-ered study to demonstrate a reduction 2. Stock CM, Downs JB: Airway pressure re- nary gas distribution in awake and anesthe-in mortality or ventilator days with tized-paralyzed man. J Appl Physiol 1977; lease ventilation. Crit Care Med 1987; 15:APRV compared with optimal lung pro- 462– 466 42:391– 402tective conventional ventilation has not 3. Sydow M, Burchardi H, Ephraim E, et al: 9. Tokics L, Hedenstierna G, Svensson L, et al:yet been performed. APRV (combined Long-term effects of two different ventila- V/Q distribution and correlation to atelec-with tube compensation software) re- tory modes on oxygenation in acute lung tasis in anesthetized paralyzed humans.mains unique among potential “open injury. Comparison of airway pressure re- J Appl Physiol 1996; 81:1822–1833Crit Care Med 2005 Vol. 33, No. 3 (Suppl.) S237
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