Care Medicine Volume 24 Number 4 High...

Analytic Reviews

High-Frequency Oscillatory Ventilation(HFOV) and Airway Pressure ReleaseVentilation (APRV): A Practical Guide

S. P. Stawicki, MD, Munish Goyal, MD, and Babak Sarani, MD, FACS

Despite advances in ventilator management, 31% to38% of patients with adult respiratory distress syn-drome (ARDS) will die, some from progressive respira-tory failure. Inability to adequately oxygenate patientswith severe ARDS has prompted extensive efforts toidentify what are now known as alternative modes ofventilation including high-frequency oscillatory venti-lation and airway pressure release ventilation. Bothmodalities are based on the principles of the open-lungconcept and aim to improve oxygenation by keeping thelung uniformly inflated for an extended period of time.

Although a mortality benefit has not been proven, somepatients may benefit from these alternative modes ofventilation as rescue measures while the underlyingprocess resolves. The purpose of this article is to reviewthe evidence and mechanisms underlying each modal-ity and to describe the fundamental steps in initiating,adjusting, and terminating these modes of ventilation.

Keywords: alternative mechanical ventilation; openlung; APRV; HFOV

Introduction

Inability to adequately oxygenate patients with acutelung injury (ALI) or adult respiratory distress syn-drome (ARDS) has prompted extensive efforts toidentify what are now known as alternative modesof ventilation. Animal studies demonstrate thatmechanical ventilation with large tidal volumes andhigh airway pressures leads to severe alterations inpermeability, pulmonary edema, and diffuse alveolardamage similar to the pathologic findings character-istic of ARDS.1,2 Mechanisms thought to be involvedin ventilator-induced lung injury (VILI) include

excessive stretch of the alveoli (volutrauma), shearinjury due to repetitive alveolar collapse and reopen-ing (atelectrauma), and excessive pressure within thealveoli (barotrauma).

Application of low tidal volume/low plateau pres-sure strategies during conventional ventilation inadults with ALI or ARDS results in decreased dura-tion of mechanical ventilation and mortality relativeto high tidal volume/high plateau pressure ventila-tion.3,4 However, 31% to 38% of patients proceedto die, some from progressive respiratory failure,indicating that conventional ventilation with lungprotective strategies may not be adequate.3,4

Although a mortality benefit has not been proven,such patients may benefit from alternative modesof ventilation as rescue measures to maintain oxyge-nation while the underlying process resolves.

High-frequency oscillatory ventilation (HFOV)and airway pressure release ventilation (APRV) are2 commonly used alternative modes of mechanicalventilation in this patient population. Both modal-ities are based on the principles of the open-lungconcept (OLC) and aim to improve oxygenation by

From the Division of Traumatology and Surgical Critical Care,Departments of Surgery (SPS, MG, BS) and Emergency Medi-cine (MG), University of Pennsylvania School of Medicine, Phila-delphia, Pennsylvania.

Received October 29, 2007, and in revised form April 28, 2008.Accepted for publication May 05, 2008.

Address correspondence to: Babak Sarani, 3440 Market Street,First Floor, Philadelphia, PA 19104; e-mail: [email protected].

215

Journal of Intensive

Care Medicine

Volume 24 Number 4

July/August 2009 215-229

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J Intensive Care Med OnlineFirst, published on July 17, 2009 as doi:10.1177/0885066609335728

keeping the lung uniformly inflated for an extendedperiod of time. The OLC was originally coined byLachmann in 1992 and highlights the importanceof maintaining open alveoli while minimizing over-distension and atelectrauma.5 In general, eithermode could be considered when the fraction ofinspired oxygen (FiO2) is greater than 60%, positiveend-expiratory pressure (PEEP) is greater than15 cm H2O, plateau pressure is greater than 30 cmH2O, and the arterial oxygen saturation is less than90%.6

The purpose of this article is to review the evi-dence and mechanisms underlying each modalityand to describe the fundamental steps in initiating,adjusting, and terminating these modes of ventila-tion. Discussion is limited to adult patients. It isassumed that the reader has a sound understandingof the pathophysiology of ARDS and VILI.

High-Frequency Oscillatory Ventilation

High-frequency oscillatory ventilation has beenidentified as an alternative method of applying lowtidal volume, controlled pressure ventilation in thesetting of ARDS.7 Traditionally used with great suc-cess in neonatology, HFOV has recently been

recognized as potentially useful in adult patientswith ARDS.7 Its use in adults is based on the hopethat it will improve oxygenation without furtherinjuring the lung. The only HFOV approved for usein adults is the Sensormedics 3100B (Viasys Health-care, Yorba Linda, CA).

Rationale Behind HFOV

Patients who develop ARDS or ALI have reducedlung compliance and impaired oxygenation.8 High-frequency oscillatory ventilation attempts to dealwith potential risks of mechanical ventilation, baro-trauma, volutrauma, atelectrauma, and oxygen toxi-city and can be considered when conventionalventilation fails to safely and adequately providerespiratory support. High frequency ventilation isgenerally considered beneficial for patients withsevere pulmonary failure because (a) it uses muchsmaller tidal volumes than conventional ventilation,(b) it maintains the lungs/alveoli open on the defla-tion limb of the pressure-volume curve (Figure 1)at a relatively constant airway pressure and thus mayprevent atelectrauma and barotrauma,9 and (c) itimproves ventilation/perfusion (V/Q) matching byensuring uniform aeration of the lung.9 It is possible

Figure 1. Pressure-volume curve comparing regions of ventilation using high-frequency oscillatory ventilation (HFOV) and airwaypressure release ventilation (APRV). Note that ventilation with HFOV occurs on the expiratory limb, whereas ventilation with APRVoccurs on the inspiratory limb of the curves.

216 Journal of Intensive Care Medicine / Vol. 24, No. 4, July/August 2009

that adults with severe ARDS may benefit from HFOVdue to the long and variable time constant required forfilling of noncompliant alveoli. Such alveoli may expe-rience atelectrauma even with low tidal volume, mod-erate PEEP conventional ventilation. Similarly, lessfibrotic segments of the lung may experience cyclicvolutrauma due to preferential air flow into these seg-ments with conventional ventilation. Various studieshave used different criteria for determining whenHFOV should be instituted in adults, but a consensusarticle that sought to adhere to lung protectivestrategies of mechanical ventilation while maintainingadequate gas exchange, suggested its use when conven-tional ventilator settings require an FiO2 greater than70% and PEEP greater than 14 cm H2O or when thearterial pH is less than 7.25 with a tidal volume that isgreater than 6 cm3/kg and a plateau pressure that isgreater than 30 cm H2O.10

Several studies in adults have shown that oxyge-nation improves after implementation of HFOV, butmortality benefit has not been demonstrated inrandomized trials.11,9,12-14 However, these studieswere not powered sufficiently to detect smallchanges in mortality. In a study by Fort et al,9 HFOVwas evaluated in terms of safety and effectivenessin patients with ARDS.9 This prospective studyincluded patients with mean peak inspiratory pres-sure of 54.3 + 12.7 cm H2O, PaO2/FiO2 ratio of68.6 + 21.6, and PEEP of 18.2 + 6.9 cm H2O.High-frequency oscillatory ventilation was institutedafter varying periods of conventional ventilation(5.12 + 4.3 days). A lung volume recruitment strat-egy was used concurrently. During the study, 76% of

patients demonstrated improved gas exchange andan overall improvement in PaO2/FiO2 ratio. Cardiacoutput was not compromised in any of the patientsdespite increases in mean airway pressure, lendingcredence to the fact that HFOV is both a safe andan effective means to augment oxygenation in adultpatients with severe ARDS failing conventional ven-tilation. Thus, patients who need maximal alveolarrecruitment to keep the FiO2 below toxic levels maybenefit from HFOV.

Mechanics of High-Frequency OscillatoryVentilation

The variables that are controlled directly on the3100B ventilator are respiratory frequency, ampli-tude of ventilation (also called the power or DP),mean airway pressure (Paw), bias gas flow rate, per-centage of inspiratory time, and FiO2. Suggested ini-tial ventilator settings are noted in Table 1. The coreof the HFOV system consists of a piston assemblythat incorporates an electronic control circuit, orsquare-wave driver, which powers a linear drivemotor (Figure 2). This motor consists of an electricalcoil within a magnet, similar to a permanent magnetspeaker. When a positive polarity is applied to thesquare-wave driver, the coil is driven forward. Thecoil is attached to a rubber bellows, or diaphragm,to create a piston. When the coil moves forward, thepiston moves forward, resulting in the creation of theinspiratory phase. When the polarity becomes nega-tive, the electrical coil and the attached piston are

Table 1. Suggested Initial Settings for APRV and HFOV

HFOV10 APRV

Frequency Thigh 4-6 secondspH < 7.1 4 Hz Tlow 0.6-0.8 seconds based on T-PEFRa

pH 7.1-7.19 5 Hz Phigh Same as plateau pressure on CV orPaw þ 2-4 cm H2O if transition from HFOV

pH 7.2-7.35 6 Hz Plow 0pH > 7.35 7 Hz FiO2 100%

Amplitude (power) 70-90 cm H2OPaw 5 cm H2O > plateau pressure on

CV to max of 35 cm H2OBias flow 40 L/minInspiratory time 33%FiO2 100%

NOTES: APRV ¼ airway pressure release ventilation; CV ¼ conventional ventilation; HFOV ¼ high-frequency oscillatory ventilation;Paw, mean airway pressure.a Tlow may have to be greater than 1 second in patients with severe obstructive lung disease.

Review of Open-Lung Ventilation / Stawicki et al 217

driven away from the patient, creating the expiratoryphase. By moving rapidly, the diaphragm oscillates aconstant stream of gas, called the bias gas flow,through the airways. It is recommended that the lungbe aggressively recruited prior to the start of HFOVto ensure that all the potentially recruitable alveoliare open.

The speed of oscillation is set by manipulatingthe frequency (Figure 3). One Hertz is equal to 1breath per second, that is, 60 breaths per minute.A frequency of 5 Hz gives a frequency of 5 breathsper second or 300 breaths per minute. An important

point to remember is that given a fixed inspiratory toexpiratory time ratio, as frequency is increased, theexcursion of the piston is limited by the time allo-cated for each breath cycle. Therefore, changes infrequency are inversely proportional to the amplitudeand thus delivered tidal volume (see below). Alveoliwith short-time constants for air flow (high lungcompliance and low airway resistance) can be venti-lated more effectively at higher frequencies thanthose which have longer time constants (low lungcompliance or high airway resistance). Frequencyselection also directly affects the pressure cycles

Figure 2. Basic design of the high frequency oscillating ventilator. A bias gas flow is moved rapidly by a piston-driven assembly.

Figure 3. Waveforms depicting the key variables that are controlled during high frequency oscillation as compared to conventionalventilation. The y-axis on the left depicts changes in airway pressure seen with high frequency oscillatory ventilation and the y-axis onthe right depicts changes in peak airway pressure with conventional ventilation. Note that tracheal pressure becomes negative at peakexpiration, thereby making expiration an active process. Also note that as amplitude increases, delivered minute ventilation increases.A background tracing of pressure versus time using a respiratory rate of 12 and inspiratory to expiratory ratio of 1:3 with conventionalventilation is presented for comparison.


applied to the lung. A smaller percentage of the cir-cuit change in pressure is transmitted at higher fre-quencies. Whereas the normal lung can beventilated over a wide pressure range without indu-cing injury, the lung with poor compliance has a verylimited zone of safety.15 As frequency increases, thezone of safe pressure widens, making it easier tomaintain more of the lung homogenously aerated.15

Unfortunately, there is no simple formula for esti-mating the ideal frequency for an individual patient,and clinical judgment combined with arterial bloodgas measurements is needed (Tables 2 and 3). Useof frequency lower than 3 Hz is not recommendedbecause the depth of oscillation increases markedly,which may result in increased risk of barotrauma. Inaddition, the frequency should not be raised higherthan 7 Hz in adults. Frequency is adjusted in 1 Hzincrements based on the PCO2 (see below).

The amount of polarity voltage (also calledpower, amplitude, or DP) applied to the electricalcoil determines the distance that the piston is driventoward/away from the patient’s airway. Therefore,increasing the polarity voltage increases the pistonmovement or amplitude. The easiest way to concep-tualize this is to view it as the means by which tidalvolumes are delivered and removed about the meanairway pressure (Figure 3). The greater the pistondisplacement, the more volume delivered to thepatient. The extent to which the amplitude increasesdepends on the resistance the piston encounters toforward movement. For example, when the oscillatoris used in a patient with low compliance or high air-way resistance, the piston meets greater pressureduring the inspiratory phase, resulting in lesserchange in the effective tidal volume. In addition, as

depicted in Figure 3, expiration is an active processin HFOV. This is because negative displacement ofthe diaphragm results in subatmospheric pressure.Generally, the starting power setting should be 70to 90 cm H2O. Most commonly, this variable isadjusted to obtain a slight wiggle to the level of thepatient’s thigh, though it has been recommendedthat the starting setting be PCO2 þ 20 cm H2O. Asdescribed below, subsequent adjustments are madebased on the PCO2.

The mean pressure adjust control mechanismallows for adjustments in Paw. This control varies theresistance placed on a mushroom-shaped controlvalve on the patient circuit at the terminus of theexpiratory limb. Following manual recruitmentefforts, increasing the Paw keeps alveoli open at aconstant pressure, thus minimizing or avoiding

Table 2. Ventilator Adjustments Based on Blood Gas Results

HFOV APRV

Hypoxemia� Increase FiO2 � Increase FiO2

� Increase Paw by 2 cm H2O to max 40 cm H2O � Recruitment maneuver� Recruitment maneuver in cases of recurrent hypoxemia � Increase Thigh

� Increase bias flow � Increase Phigh to max 40 cm H2O� Adjust Tlow to keep T-PEFR > 50%

Hypercapnea/acidemia� Decrease frequency to nadir of 3 Hz � Ensure patient is spontaneously breathing� Increase power to max 90 cm H2O � Increase Tlow

� Introduce endotracheal cuff leak � Increase Phigh and Thigh to increase minute ventilation

NOTES: APRV ¼airway pressure release ventilation; HFOV ¼ high-frequency oscillatory ventilation; FiO2 ¼ Fraction of inspiredoxygen; Paw ¼ Mean Airway Pressure; T-PEFR ¼ Terminal peak expiratory flow rate.

Table 3. Summary of Important RespiratoryTherapy and Nursing Considerations With Regard

to HFOV Use and Routine Maintenance

Perform thorough suction before connecting to the oscillatorPerform recruitment maneuver before connecting to the

oscillatorUse closed system suction catheterAvoid disconnection from the ventilatorCheck for changes in pitch/rhythm of delivered breathsCheck chest/thigh wiggle and changes in chest/thigh wiggleAlways humidify gasesIf oscillator stops during suctioning; silence alarm, pull back

catheter and restart oscillatorObtain blood gases and chest x-ray 2 hours after HFOV com-

mencement and at least daily thereafterEnsure appropriate education regarding the oscillator for rela-

tives of the patient

NOTE: HFOV ¼ high-frequency oscillatory ventilation.


atelectrauma from shearing forces. As with all formsof mechanical ventilation, increases in mean airwaypressure result in enhanced oxygenation. Althoughincreasing Paw increases the transpulmonary pres-sure, it does not affect cardiac output in euvolemicpatients.9 As discussed below, the mean pressure-adjust control is bias flow dependent. Most authorsrecommend a starting Paw 5 cm H2O above the lastplateau pressure noted during conventional ventila-tion with a maximal starting Paw of 35 cm H2O. Basedon outcome studies on conventional ventilation, thegoal is to keep the Paw less than 30 cm H2O. Meanairway pressure should be adjusted in increments of2 cm H2O based on the oxygen saturation. Patientswho have recurrent hypoxemic events that resolvewith recruitment should have their Paw increased.

Bias flow is the rate at which gas flows through theventilator circuit. The generally accepted starting biasflow rate is 40 L/min, and the maximal flow possible onthe 3100B is 60 L/min. An increase in bias gas flow willincrease Paw, thereby improving oxygenation. Themaximal flow may be needed to maintain Paw inpatients with a large air-leak, such as bronchopleuralfistulae. However, the maximal flow rate is not suffi-cient to support significant spontaneous respiratoryefforts and is one reason that patients must be deeplysedated or pharmacologically relaxed while on HFOV.

In conjunction with amplitude, mean airwayadjust, bias flow, and frequency control, the percent-age of inspiratory time can also be adjusted. Becausethe endotracheal (ET) tube contributes at least 50%of the total airway resistance during expiration, theinspiratory time setting should always be less than50% to minimize the risk of air trapping and volu-and barotraumas.16 Inspiratory time of 33% is opti-mal because it results in a drop in the mean intrapul-monary pressure as a result of higher flow-dependentET tube resistance during inspiration. This is due tohigher flow rates during the shortened inspiratoryphase.16 Increasing the inspiratory time will improveboth oxygen (by increasing Paw) and CO2 exchange(by increasing delivered tidal volume), though it canalso increase the risk of lung injury. Because of this,it is the variable least commonly altered to addressblood gas values.

Gas Exchange

Tidal volumes delivered using the 3100B are notmeasured and are estimated to be 1 to 2 cm3/kg—

approximately the volume of anatomic dead space.There are several mechanisms postulated to explaingas transport under these nonphysiologic conditions(Figure 4), and the reader is referred to more defini-tive sources for greater detail of information.17,18

Briefly, the gas transport in the most proximal airwayoccurs by convection, and gradually transitions intoa mixture of convection and diffusion and finallypurely diffusion as one progresses along the airwaytree.17 Bulk flow can still provide conventional gasdelivery to proximal alveoli with low regional deadspace volumes.18 There is also the presence of coax-ial flow, wherein the gas in the center of large air-ways and the ET tube flows inward while gas onthe periphery flows outward. This can developbecause of the asymmetric low profile of high velo-city gases.18 Dispersion phenomena can producemixing of fresh and residual gas along the flow frontof gas through a tube. Pendelluft flow refers to flowof gas between adjacent alveoli with different impe-dance, as seen in ARDS.17,18 Collateral ventilationand cardiogenic mixing also play a role.17 Finally,augmented molecular diffusion can occur at thealveolar level secondary to the added kinetic energyfrom the oscillations.16-18 The importance of eachof these mechanisms is debated, and it has been sug-gested that a combination of all the above factorsmay be in play simultaneously during HFOV.16,17,19

As with any form of mechanical ventilation, oxy-genation on HFOV can be improved by eitherincreasing the FiO2 or increasing the mean airwaypressure. As noted above, the mean airway pressurecan be increased directly or it can be adjusted byincreasing the inspiratory time. Increases in Paw

result in greater alveolar recruitment and subse-quent improvement in V/Q matching. However,increasing Paw to a point where perialveolar vesselscollapse from alveolar overdistention can result inboth seemingly paradoxical hypoxemia and/or baro-trauma to the lung. Because Paw is affected by manyvariables, such as inspiratory time or ET cuff leak(discussed below), one must be cognizant of the factthat a change in one variable may affect the othervariables and vice versa.

Ventilation on HFOV is facilitated by theextremely efficient mixing of gas in the airways. Car-bon dioxide removal is approximately proportional tothe product of oscillation frequency and the ampli-tude squared.20 Thus, changes in tidal volume havea greater impact on CO2 clearance than changes inrespiratory rate. This explains why decreasing the


frequency results in an increase in CO2 clearance—that is, decreasing the frequency results in anincrease in delivered tidal volume. Furthermore,even the smallest adjustments in amplitude orchanges in lung compliance and delivered tidal vol-ume have a great effect on ventilation. Conse-quently, CO2 elimination is controlled primarily byadjusting amplitude first and then by adjusting fre-quency.20 Lastly, ventilation can also be augmentedby decreasing the anatomic dead space. This canbe done by deflating the cuff of the ET tubesufficiently to decrease the Paw 5 to 8 cm H2O (andcompensating for this decrease by manually increas-ing the Paw again). However, this may result in anincreased risk of aspiration or derecruitment of thelung, though adverse outcomes have not beenreported in studies on adult patients.

Because there is no bulk flow of gas, significantrespiratory acidosis is common at the start of HFOV.

Patients who have significant preexisting acidemiamay need to be temporized with intravenous bufferingsolutions while CO2 exchange stabilizes. Table 4 liststhe factors associated with decreased tidal volumedelivery and thus impaired ventilation with HFOV.

To summarize, oxygenation is improved byincreasing mean airway pressure, FiO2, or percentageof inspiratory time. Ventilation (CO2 exchange) isimproved by decreasing frequency, increasing power,increasing inspiratory time, or creation of a cuff leak.The risks and benefits of changes in each variablehave to be considered. Table 2 list suggested ventila-tor adjustments based on arterial blood gas results.

Interaction With Spontaneous Breathing

Spontaneous breaths contribute useful lung reex-panding forces.21,22 Much like in APRV, spontaneous

Figure 4. Possible mechanisms to account for gas exchange at various levels of the bronchoalveolar tree during high frequencyoscillation.


breaths on HFOV help maintain end-expiratory alveo-lar expansion in dependent lung regions and improveV/Q distributions.23,24 A significant reduction in dayson ventilator was observed when spontaneous breath-ing efforts were allowed in patients with ALI/ARDS.22

However, vigorous spontaneous respiratory efforts,especially in large size patients, may contribute tosudden pressure variations that activate equipmentalarms, interrupt oscillations, and produce significantoxygen desaturation. It is for this reason that the earlyHFOV trials in adults recommended administrationof muscular blockade. Current sedation protocolsattempt to maintain the patient’s ability to breathespontaneously with small tidal volumes while sup-pressing deep breaths or coughing, thus minimizingpotential complications related to myopathy/neuropa-thy of prolonged neuromuscular blockade.25,26

Weaning From HFOV

There is no consensus on how to wean patients fromHFOV to conventional ventilation. However, a pro-tocol used in 2 randomized trials called for the Paw

to decrease in increments of 2 cm H2O to a goal of30 cm H2O after the FiO2 had been weaned to lessthan 60%.13,14 The FiO2 was then weaned to 40%if the oxygen saturation (SaO2) remained greater than88%. Finally, the Paw was weaned again to a finalgoal of 20 to 25 cm H2O. The patient was then tran-sitioned to a lung protective volume-controlled modeof ventilation if the SaO2 remained greater than 88%for 24 hours. Initial conventional ventilation settingswere designed to ensure that the mean airway pres-sure remained 20 to 25 cm H2O. The patient wasconsidered to fail this transition and was convertedback to HFOV if the SaO2 decreased to less than88% in the first 48 hours following transition. Thisprotocol is supported by other studies that suggestthat weaning the Paw to less than 20 cm H2O prior

to transitioning to conventional ventilation can causederecruitment of alveoli and hypoxemia.25 Ininstances where the initial Paw is greater than 35 cmH2O and the FiO2 is greater than 60%, some authorssuggest weaning the Paw and FiO2 concurrently to tryto minimize excess stretch and barotrauma on thealveoli as quickly as possible. In these instances, thePaw should be weaned to 35 cm H2O initially, thenthe FiO2 should be weaned to less than 60%, and thenthe protocol outlined above can be followed.

Complications and Drawbacks of HFOV

Despite research showing benefits of HFOV, use ofoscillatory ventilation is rare in adult patients, andcomfort level is generally low among medical person-nel using this equipment,27 consequently resultingin difficulty with troubleshooting and adjusting theventilator. Possible complications include overdis-tention/underdistention of the lung, pneumothorax,ET occlusion from secretions, and hemodynamiccompromise. Other limitations include inability totransport the patient and deliver nebulizedmedications.

The possibility of lung overdistention on HFOVdue to trapping of gas has been investigated.28

Because this cannot be measured directly, the exactextent to which this is a problem is controversial, butthere is no difference in the reported rate of pneu-mothorax between HFOV and conventional ventila-tion.13.Lung underdistention can also be a problemunder HFOV. Although controversial, small tidalvolumes delivered at a constant mean airway pres-sure may actually exacerbate or result in progressiveatelectasis, one of the problems HFOV is thought toovercome. This underscores the importance ofrecruiting the lung at the start of HFOV.

Continuous positive intrathoracic pressureimpedes venous return to the heart and thereforecardiac output. This can result in hypotension whenpatients are transitioned from conventional ventila-tion to HFOV. Patients must be euvolemic prior toinitiation of HFOV to minimize this risk, and thebedside practitioner should be ready to volumeresuscitate the patient as needed. As previouslydescribed, systemic hypotension may also be wor-sened by transient acidemia.

Metered dose inhalers are largely ineffective dur-ing HFOV, with only about 25% of a nebulized med-ication being detectable at the end of the ET tube.29

Table 4. Factors Contributing to Decreased TidalVolume Delivery With HFOV

Decreased endotracheal tube diameterMucous plug or alveolar edema fluid accumulationDecreased ventilator power or amplitudeDecreased percentage of inspired timeDecreased respiratory system complianceIncreased endotracheal tube lengthIncreased ventilator frequency

NOTE: HFOV ¼ high frequency oscillatory ventilation.


Better methods to deliver aerosolized medicationswith HFOV are being developed.

Patient transport during HFOV may be a signif-icant logistical problem because there is no portableversion of the equipment. However, an effective pro-tocol for transport of patients on HFOV has beendescribed.7 This mechanism involves clamping theET tube while on HFOV, transition to a self-inflatingbag with 20 cm H2O PEEP valve, unclamping of theET tube with vigorous manual ventilation duringtransport, and reversal of these procedures once anoscillatory ventilator has been set up at the trip des-tination.7 Recruitment maneuvers can be used asneeded to reestablish oxygenation. This protocol not-withstanding transport of such patients is potentiallydangerous and should be minimized.

Unique Aspects Regarding HFOV

There are a number of specific respiratory therapyand nursing aspects that should be highlighted withregards to patients on HFOV (Table 3). The sight ofsomeone being ‘‘oscillated’’ can be disturbing for thefamily and friends of the patient. Hence, it is impor-tant to ensure adequate education regarding expecta-tions provided to the patient’s family and friends.

It is difficult to appropriately auscultate thechest while a patient is on HFOV. Physicians andnurses must rely on chest x-ray and objective mea-sures (eg, vital signs, ventilator readings, and bloodgas analysis) to detect new lung pathology. Dailychest x-ray is needed to ensure adequate lungexpansion.

A closed system suction unit should be used onHFOV because disconnecting the patient to suctioncan potentially lead to derecruitment. Unless other-wise indicated, suctioning for the first 24 hours isnot necessary. When using a closed system suctionsystem, it is important to draw back the suctioncatheter all the way from the ET tube upon comple-tion. Ideally, the patient should be thoroughly suc-tioned before HFOV is commenced. Once thepatient is oscillated, every attempt must be made totry not to disconnect the patient from the oscillatorto prevent derecruitment.

All clinical staff need to be trained in recognitionof HFOV-related complications. This is especiallyimportant with HFOV because the ventilator ispoorly alarmed to alert the bedside staff to possiblecomplications. Clinical assessment and experience

are needed to recognize ET tube obstruction(increase in amplitude with an increase in Paw,decrease in SpO2, and increase in PCO2), tensionpneumothorax (decrease in SpO2, disparity in theheight of the left and right chest walls, and a fall inblood pressure), or pulmonary overdistension (fallin blood pressure, increased central venous pressure,and decreased SpO2). Observation of the patient forequal and continuous chest wiggle should be per-formed upon initiation of HFOV and followedclosely thereafter. Chest wiggle diminishes if theET tube has moved or is obstructed. Chest wiggleon one side only may indicate that the patient hasdeveloped a pneumothorax or has a main-stem intu-bation. Chest wiggle assessments should be per-formed following any patient repositioning.

Airway Pressure Release Ventilation

Airway pressure release ventilation representsanother open-lung mechanical ventilation strategy.Airway pressure release ventilation was designedto provide the oxygenation benefits of a near-permanent recruitment maneuver, while augment-ing ventilation for patients with low-compliance lungdisease.30 Stock et al31 were first to describe APRVin 1987 and are credited with its introduction.

Airway pressure release ventilation has beendescribed as continuous positive airway pressure(CPAP) with regular, brief, intermittent releases inairway pressure.30 It can therefore be thought of asa time-cycled, pressure-limited mode of mechanicalventilation, which operates by cycling between 2pressure levels within a high-flow (demand-valve)CPAP circuit that allows spontaneous breathing atany phase of the ventilatory cycle. This mechanismmay reduce the need for heavy sedation31-33 andrequires patient involvement, thus precluding theuse of paralysis.

The degree of ventilatory support with APRV isdetermined by the duration of the 2 CPAP levels andthe distending pressure used to recruit alveoli witheach mechanical cycle.31,34 The tidal volume gener-ated depends mainly on respiratory compliance andthe difference between the CPAP levels; because, Plow

is usually set at zero, tidal volume is dependent onPhigh. Of interest, when spontaneous breathing isabsent, APRV is indistinguishable from inverse ratiopressure-controlled, time-cycled ventilation.31,34


Rationale Behind APRV

Lungs of patients with ALI/ARDS are often charac-terized by heterogeneity of threshold opening pres-sures across different lung areas.35 The cyclicchange in pressure and tidal volume that is charac-teristic of conventional ventilation may preferentiallyfill and overdistend alveoli with a short-time con-stant for filling (ie, nonfibrotic alveoli) while indu-cing atelectrauma in fibrotic alveoli with a longertime constant for filling. Airway pressure releaseventilation aims to minimize this risk by keeping thelung inflated for an extended period of time whileminimizing the exhalation (or release) phase.

Compared to conventional ventilation, APRV isassociated with significantly lower peak/plateau air-way pressures for a given tidal volume.30 In a multi-center, prospective crossover trial of patients withALI, Rasanen et al36 demonstrated a 55% reductionin peak airway pressures compared with conven-tional ventilation while maintaining similar oxygena-tion and ventilation. By keeping the lung expandedfor an extended period of time and allowing minimaltime for exhalation, APRV may produce nearlycomplete recruitment while minimizing lowervolume-induced lung injury associated with cyclicrecruitment and atelectrauma.30 However, asopposed to HFOV, APRV allows for a brief exhala-tion period. It is known that ARDS is a heteroge-neous process whereby less fibrotic regions of thelung receive inspiratory flow preferentially while lesscompliant alveoli collapse earlier during exhalation.Therefore, APRV could theoretically cause VILI byinducing volutrauma during the inhalation phaseand atelectrauma during the release phase inpatients with ARDS. As discussed below, ventilatoradjustments based on the flow-versus-time andpressure-versus-time curves are needed to minimizethis risk.

There is evidence that points to importantdifferences between ventilation distribution duringspontaneous breathing and controlled mechanicalventilation.37 During spontaneous breathing, the pos-terior muscular sections of the diaphragmatic musclemove more than the anterior tendon plate. Thus, in asupine patient, the dependent portions of the lungsare better ventilated during spontaneous breathing.Because in conventional methods of ventilation thediaphragm remains more passive, and because of thecomplex interactions between abdominal and

thoracic forces, mechanical ventilation tends to bedistributed more towards the anterior, nondependent,and relatively less perfused areas of the lung.38 Paraly-sis and heavy sedation further inhibit diaphragmaticcontraction leading to cephalad migration and furthercompression of dorsal inferior lung parenchyma.Therefore, more atelectasis is observed in the dorsallung areas, which are closer to the diaphragm. Byrecruiting alveoli and reestablishing functional resi-dual capacity at a more favorable point on the pres-sure-volume curve, APRV can ‘‘unload’’ inspiratorymuscles and decrease the work of breathing associ-ated with acute restrictive lung disease.39 Sponta-neous breathing, therefore, might require less effort.The ability to have variable gas flow and accommodatespontaneous ventilation is a key difference betweenHFOV and APRV. Spontaneous breathing with APRVin experimental lung injury models was associatedwith less atelectasis by computed tomographic evi-dence.40 Furthermore, Neumann et al41 demon-strated that allowing spontaneous breathing withAPRV decreased intrapulmonary shunt by increasingventilation of aerated-dependent lung tissue andopening atelectatic lung parenchyma.41

Although relatively weak, there is evidence thatuse of APRV may be associated with decreases inmultiorgan failure and perhaps mortality (whencompared to mortality in the ARDSNet trial),4,35 aswell as significant decrease in the need for sedativesas compared to volume-controlled ventilation inpostcardiac surgery patients.42 Furthermore, whencompared to pressure-controlled ventilation, APRVhas been associated with higher cardiac index andlower systemic and pulmonary vascular resis-tance.33,43 In early clinical studies, APRV wasdemonstrated to be a feasible alternative to conven-tional mechanical ventilation in patients with ALIof mild-to-moderate severity.36

Mechanics of APRV

The 5 major parameters that need to be adjustedwhen using APRV are FiO2, Phigh (high pressure),Thigh (time spent at the high pressure), Plow (lowpressure), and Tlow (time spent at the low pressure).The Phigh and Thigh are the main determinants ofmean airway pressure and thus are directly corre-lated with oxygenation.35 Because mean airway pres-sure also directly correlates with mean alveolar


volume (thus alveolar-capillary diffusion surfacearea), Phigh and Thigh are directly related to gasexchange. The pressure gradient between Phigh andPlow, Tlow, and the patient’s spontaneous minute ven-tilation are the main determinants of alveolar venti-lation, thus, CO2 clearance. Suggested initialventilator settings are noted in Table 1.

The Plow and Tlow regulate end-expiratory lungvolume and should be optimized to prevent alveolarclosure and associated derecruitment while maximiz-ing alveolar ventilation. Generally, the majority(80%-95%) of the total cycle time (Thigh þ Tlow)should be spent at Phigh to optimize mean alveolar

volume and thus maximize potential gas exchange.To minimize derecruitment, the Tlow should be setsuch that expiration ends when expiratory flowequals 50% to 75% of peak expiratory flow rate(PEFR; Figure 5). Because the flow curve shownon the ventilator is a summation of all alveoli, it ispossible that severely fibrotic alveoli with a short-time constant for exhalation will collapse and sustainatelectrauma if exhalation time is extended. More-over, VILI may be possible even with this recom-mended exhalation time.

Newly intubated adult patients who are started onAPRV should have their Phigh set at the desired plateau

Figure 5. Pressure versus time and flow versus time graphs seen with airway pressure release ventilation. Note that spontaneousbreaths are present during the respiratory cycle. Furthermore, note that Tlow is set such that end-expiratory flow is 50% to 60% ofpeak expiratory flow.


pressure. If a patient is transitioning from conven-tional ventilation, their Phigh should be set at theirmostrecent plateau pressure (usually 20-35 cm H2O).When transitioning from HFOV to APRV, the patientshould be placed on Phigh equal to mean Paw plus 2 to4 cm H2O.35 Regardless of when the patient was intu-bated or prior mode of ventilation, Plow is set at 0 cmH2O, Thigh between 4 and 6 seconds, and Tlow between0.6 and 0.8 seconds based on the expiratory flow mea-surements.35 Pressurelow is set to zero to optimize thepressure gradient during the release phase, thus maxi-mizing exhalatory flow and alveolar ventilation.Despite the set Plow, the release phase (Tlow) is verybrief, preventing an airway pressure of zero. Timelow

is kept brief to prevent actual alveolar collapse or dere-cruitment. Of note, patients with obstructive lung dis-ease should have their initial Tlow set between 0.8 and1.5 seconds and adjusted based on the expiratory flowmeasurements.35 In both scenarios, the pressure-timecurve can be used to confirm that the airway pressurenever reaches zero.

Special Measured Parameters

The PEFR is the maximal expiratory flow rateachieved during the release phase of APRV. It is afunction of the pressure gradient between Phigh andPlow, lung volume, compliance of the lung andthorax, and the airway resistance. Peak expiratoryflow rate termination (T-PEFR) is a measured para-meter that represents the expiratory flow rate at theend of the release phase of the APRV cycle. Peakexpiratory flow rate termination is useful in guidingAPRV adjustments, when used as a ratio of PEFR.35

To keep things practical, a ratio of T-PEFR to PEFRof 60% is ideal. However, because of individualvariability, a ratio between 50% and 66% may beused successfully (Figure 5).

Gas Exchange

As with HFOV, a large part of gas exchange occursthrough convection and diffusion during the inspira-tory phase of APRV. Alveolar recruitment results inimproved V/Q matching, intrapulmonary shunting,and arterial oxygenation relative to conventional ven-tilation.23 The increase in arterial oxygenation sup-ports the notion of ongoing recruitment ofpreviously nonventilated lung areas, especially when

coupled with improved pulmonary compliance. Theimprovement in oxygenation occurs gradually overa period of 24 hours and results from gradual pul-monary recruitment.44

As with all modes of ventilation, oxygenation isincreased by increasing the FiO2 or the mean airwaypressure. The mean airway pressure in APRV isincreased by increasing the Phigh or the Thigh. Increas-ing the Phigh beyond 30 cm H2O risks inducingbarotrauma, however, may be indicated in patientswith poor thoracic or abdominal compliance.35

Airway pressure release ventilation is capable ofeither augmenting alveolar ventilation in the sponta-neously breathing patient or facilitating ventilationin the apneic patient.45 In fact, APRV was initiallydescribed as an improved method of ventilatory sup-port in the presence of ALI and hypercarbia.31 Air-way pressure release ventilation augments CO2

removal by improving V/Q matching and decreasingintrapulmonary shunting. A limiting factor for car-bon dioxide clearance is the gradient between alveo-lar and arterial CO2. This gradient is refreshedduring the ‘‘release’’ phase of APRV when fresh gasis exchanged in the alveolar tree. The optimal releasefrequency is variable and depends upon a number offactors including CO2 production, V/Q mismatch,shunt, and cardiac output. As noted above, CO2

exchange may decrease as the Thigh increasesbecause the respiratory frequency decreases.35 Thisphenomenon is similar to that observed withdecreased CO2 clearance with increasing I:E ratios.

Although the bulk of CO2 exchange occursduring the release phase, other mechanisms suchas cardiogenic mixing and spontaneous breathingalso affect on alveolar ventilation. Cardiogenic mix-ing results in CO2 movement toward central airwaysduring the Thigh (or breath-hold) period, improvingthe ventilatory effectiveness of the release.46 Theaddition of spontaneous breaths during the Thigh

period further enhances recruitment and ventilationefficiency.35 Manipulation of Thigh must be tailoredto each patient because of the number of factorsinvolved with CO2 removal. Table 2 lists recom-mended ventilator adjustments based on blood gasresults.

Weaning From APRV

Patients with adequate or improving oxygenationwhile on APRV can be progressively weaned by


lowering the Phigh and extending the Thigh. As aresult, the number of timed releases is decreased andthe machine minute ventilation is reduced. Thisforces the patient to increase spontaneous minuteventilation to maintain constant total minute ventila-tion. This can be equated to a progressive sponta-neous breathing trial and a relatively ‘‘smooth’’transition toward CPAP. Some authors believe thatthe ultimate weaning target of APRV is CPAP, andthat pressure-assisted breathing (pressure support)may actually be counter-productive.35 Patients canbe transitioned back to conventional ventilationwhen the Phigh is less than 20 cm H2O, the Thigh isgreater than 6 seconds, and the FiO2 is less than40%. Although it has not been studied, transitioningto conventional ventilation may expedite weaning inan environment where care providers are not asfamiliar with APRV.

Complications and Drawbacks of APRV

In general, APRV is not indicated in patients who arenot breathing spontaneously. Although APRV canoxygenate adequately in the absence of spontaneousbreathing, the patient’s spontaneous breaths contrib-ute a significant amount of the total minute ventila-tion. Because many of the proposed advantages ofAPRV (improved gas exchange, reduced dead space,possible decreased requirement for sedation andanalgesia, and improved hemodynamics) are thoughtto be due to the preservation of spontaneous breath-ing, the absence of spontaneous breathing rendersbenefits of APRV relatively ineffective.47

As with HFOV, intravascular volume often needsto be augmented in patients on APRV to offset thedecrease in venous return to the heart, which resultsfrom prolonged positive intrathoracic pressure.However, as opposed to HFOV, these cardiovascularside effects may be minimized on APRV by reducingmechanical ventilation to a level that provides ade-quate support for existing spontaneous breathingwhile avoiding overly high levels of positive airwaypressure.48 Periodic reduction of intrathoracic pres-sure achieved by maintaining spontaneous breathingduring mechanical ventilation promotes venousreturn to the heart and increased cardiac output andoxygen delivery.49 Moreover, the periodic release ofpositive intrathoracic pressure also augments venousreturn to the heart.

Other relative contraindications to APRVinclude patients with severe obstructive pulmonaryconditions who are unable to empty their lungs inless than 2 seconds.18 This group includes patientswith severe asthma and chronic obstructive pulmon-ary disease (COPD).

Conclusion

Both HFOV and APRV have been shown to improveoxygenation in patients with ARDS. The importantdifference between APRV and HFOV is that APRVallows spontaneous ventilation via an elaboratepressure-release valve mechanism, while HFOV isoften incompatible with spontaneous breathing.Consequently, APRV may be associated withreduction in the need for or degree of sedation andtherefore may be associated with decreased numberof ventilator days. Conversely, HFOV aims to keepthe lung open at all times, has less of a theoreticalchance of causing VILI by inducing volu- oratelectrauma, and mandates sedation. Lastly, APRVventilators are battery powered and therefore can beused during patient transport. This can be a distinctadvantage for patients who need ongoing interven-tion or testing. To date, there has not been eitherequivalency or superiority studies comparing these2 modalities.

A series of randomized, prospective studies areneeded to compare outcomes from use of either mod-ality both as initial therapy for evolving ARDS and asrescue modalities for patients who fail accepted con-ventional ventilation strategies. It is possible thateither APRV or HFOV may be equivalent to (if notsuperior to) low tidal volume and moderate PEEPventilation due to the concerns regarding ongoingvolu- and atelectrauma described above.

References

1. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation

pressure pulmonary edema. Respective effects of high air-

way pressure, high tidal volume, and positive end-expira-

tory pressure. Am Rev Respir Dis. 1988;137(5):

1159-1164.

2. Webb HH, Tierney DF. Experimental pulmonary edema

due to intermittent positive pressure ventilation with high

inflation pressures. Protection by positive end-expiratory

pressure. Am Rev Respir Dis. 1974;110(5):556-565.


3. Amato MB, Barbas CS, Medeiros DM, et al. Effect of a

protective-ventilation strategy on mortality in the acute

respiratory distress syndrome. N Engl J Med. 1998;

338(6):347-354.

4. Ventilation with lower tidal volumes as compared with

traditional tidal volumes for acute lung injury and the

acute respiratory distress syndrome. N Engl J Med.

2000;342(18):1301-1308.

5. Lachmann B. Open up the lung and keep the lung open.

Intensive Care Med. 1992;18(6):319-321.

6. Hemmila MR, Napolitano LM. Severe respiratory

failure: advanced treatment options. Crit Care Med.

2006;34(9 suppl):S278-S290.

7. Cartotto R, Ellis S, Gomez M, Cooper A, Smith T. High

frequency oscillatory ventilation in burn patients with

the acute respiratory distress syndrome. Burns. 2004;

30(5):453-463.

8. Simma B, Fritz M, Fink C, Hammerer I. Conventional

ventilation versus high-frequency oscillation: hemody-

namic effects in newborn babies. Crit Care Med.

2000;28(1):227-231.

9. Fort P, Farmer C, Westerman J, et al. High-frequency

oscillatory ventilation for adult respiratory distress syn-

drome—a pilot study. Crit Care Med. 1997;25(6):937-947.

10. Fessler H, Derdak S, Ferguson N, et al. A protocol for

high-frequency oscillatory ventilation in adults: results

from a roundtable discussion. Crit Care Med.

2007;35(7):1649-1654.

11. Bollen CW, van Well GT, Sherry T, et al. High frequency

oscillatory ventilation compared with conventional

mechanical ventilation in adult respiratory distress syn-

drome: a randomized controlled trial [ISRCTN24242669].

Crit Care. 2005;9(4):R430-R439.

12. Derdak S, Mehta S, Stewart TE, et al. High-frequency

oscillatory ventilation for acute respiratory distress syn-

drome in adults: a randomized, controlled trial. Am J

Respir Crit Care Med. 2002;166(6):801-808.

13. Ferguson ND, Chiche JD, Kacmarek RM, et al. Combin-

ing high-frequency oscillatory ventilation and recruit-

ment maneuvers in adults with early acute respiratory

distress syndrome: the Treatment with Oscillation and

an Open Lung Strategy (TOOLS) Trial pilot study. Crit

Care Med. 2005;33(3):479-486.

14. Mehta S, Lapinsky SE, Hallett DC, et al. Prospective

trial of high-frequency oscillation in adults with acute

respiratory distress syndrome. Crit Care Med.

2001;29(7):1360-1369.

15. Venegas JG, Fredberg JJ. Understanding the pressure

cost of ventilation: why does high-frequency ventilation

work? Crit Care Med. 1994;22(9 suppl):S49-S57.

16. Pillow JJ, Neil H, Wilkinson MH, Ramsden CA. Effect of

I/E ratio on mean alveolar pressure during high-

frequency oscillatory ventilation. J Appl Physiol. 1999;

87(1):407-414.

17. Pillow JJ. High-frequency oscillatory ventilation:

mechanisms of gas exchange and lung mechanics. Crit

Care Med. 2005;33(3 suppl):S135-S141.

18. Weavind L, Wenker O. Newer modes of ventilation: an

overview. Int J Anesthesiol. 2000;4:4.

19. MacIntyre NR. High-frequency ventilation. Crit Care

Med. 1998;26(12):1955-1956.

20. Keszler M. High frequency ventilation: evidence-based

practice and specific clinical indications. Neo Reviews.

2006;7(5):e234-e49.

21. Putensen C, Hering R, Wrigge H. Controlled versus

assisted mechanical ventilation. Curr Opin Crit Care.

2002;8(1):51-57.

22. Putensen C, Zech S, Wrigge H, et al. Long-term effects

of spontaneous breathing during ventilatory support in

patients with acute lung injury. Am J Respir Crit Care

Med. 2001;164(1):43-49.

23. Putensen C, Mutz NJ, Putensen-Himmer G,

Zinserling J. Spontaneous breathing during ventilatory

support improves ventilation-perfusion distributions in

patients with acute respiratory distress syndrome. Am J

Respir Crit Care Med. 1999;159(4 pt 1):1241-1248.

24. Wrigge H, Zinserling J, Neumann P, et al. Spontaneous

breathing improves lung aeration in oleic acid-induced

lung injury. Anesthesiology. 2003;99(2):376-384.

25. Derdak S. High-frequency oscillatory ventilation for

acute respiratory distress syndrome in adult patients.

Crit Care Med. 2003;31(4 suppl):S317-S323.

26. Higgins J, Estetter B, Holland D, Smith B, Derdak S.

High-frequency oscillatory ventilation in adults: respira-

tory therapy issues. Crit Care Med. 2005;33(3 suppl):

S196-S203.

27. Duval EL, Markhorst DG, Gemke RJ, van Vught AJ.

High-frequency oscillatory ventilation in pediatric

patients. Neth J Med. 2000;56(5):177-185.

28. Boros SJ, Mammel MC, Coleman JM, et al. Neonatal

high-frequency jet ventilation: four years’ experience.

Pediatrics. 1985;75(4):657-663.

29. Lowson SM. Inhaled alternatives to nitric oxide. Crit

Care Med. 2005;33(3 suppl):S188-S195.

30. Frawley PM, Habashi NM. Airway pressure release ven-

tilation: theory and practice. AACN Clin Issues.

2001;12(2):234-246; quiz 328-329.

31. Stock MC, Downs JB, Frolicher DA. Airway pressure

release ventilation. Crit Care Med. 1987;15(5):462-466.

32. Seymour CW, Frazer M, Reilly PM, Fuchs BD.

Airway pressure release and biphasic intermittent

positive airway pressure ventilation: are they ready for

prime time? J Trauma. 2007;62(5): 1298-1308;

discussion 308-309.

33. Kaplan LJ, Bailey H, Formosa V. Airway pressure release

ventilation increases cardiac performance in patients

with acute lung injury/adult respiratory distress syn-

drome. Crit Care. 2001;5(4):221-226.


34. Baum M, Benzer H, Putensen C, Koller W, Putz G. Bipha-

sic positive airway pressure (BIPAP)—a new form of aug-

mented ventilation. Anaesthesist. 1989;38(9):452-458.

35. Habashi NM. Other approaches to open-lung ventila-

tion: airway pressure release ventilation. Crit Care Med.

2005;33(3 suppl):S228-S240.

36. Rasanen J, Cane RD, Downs JB, et al. Airway pressure

release ventilation during acute lung injury: a prospective

multicenter trial. Crit Care Med. 1991;19(10):1234-1241.

37. Froese AB, Bryan AC. Effects of anesthesia and paralysis

on diaphragmatic mechanics in man. Anesthesiology.

1974;41(3):242-255.

38. Reber A, Nylund U, Hedenstierna G. Position and shape

of the diaphragm: implications for atelectasis formation.

Anaesthesia. 1998;53(11):1054-1061.

39. Petrof BJ, Legare M, Goldberg P, Milic-Emili J,

Gottfried SB. Continuous positive airway pressure

reduces work of breathing and dyspnea during weaning

from mechanical ventilation in severe chronic obstructive

pulmonary disease. Am Rev Respir Dis. 1990;141(2):

281-289.

40. Wrigge H, Zinserling J, Hering R, et al. Cardiorespiratory

effects of automatic tube compensation during airway

pressure release ventilation in patients with acute lung

injury. Anesthesiology. 2001;95(2):382-389.

41. Neumann P, Wrigge H, Zinserling J, et al. Spontaneous

breathing affects the spatial ventilation and perfusion

distribution during mechanical ventilatory support. Crit

Care Med. 2005;33(5):1090-1095.

42. Rathgeber J, Schorn B, Falk V, Kazmaier S, Spiegel T,

Burchardi H. The influence of controlled mandatory

ventilation (CMV), intermittent mandatory ventilation

(IMV) and biphasic intermittent positive airway pressure

(BIPAP) on duration of intubation and consumption of

analgesics and sedatives. A prospective analysis in 596

patients following adult cardiac surgery. Eur J Anaesthe-

siol. 1997;14(6):576-582.

43. Hering R, Peters D, Zinserling J, Wrigge H, von

Spiegel T, Putensen C. Effects of spontaneous

breathing during airway pressure release ventilation

on renal perfusion and function in patients with

acute lung injury. Intensive Care Med. 2002;28(10):

1426-1433.

44. Sydow M, Burchardi H, Ephraim E, Zielmann S,

Crozier TA. Long-term effects of two different

ventilatory modes on oxygenation in acute lung injury.

Comparison of airway pressure release ventilation and

volume-controlled inverse ratio ventilation. Am J Respir

Crit Care Med. 1994;149(6):1550-1556.

45. Garner W, Downs JB, Stock MC, Rasanen J. Airway

pressure release ventilation (APRV). A human trial.

Chest. 1988;94(4):779-781.

46. Engel LA, Menkes H, Wood LD, Utz G, Joubert J,

Macklem PT. Gas mixing during breath holding studied

by intrapulmonary gas sampling. J Appl Physiol.

1973;35(1):9-17.

47. Branson RD, Johannigman JA. What is the evidence base

for the newer ventilation modes? Respir Care. 2004;

49(7):742-760.

48. Kirby RR, Perry JC, Calderwood HW, Ruiz BC,

Lederman DS. Cardiorespiratory effects of high positive

end-expiratory pressure. Anesthesiology. 1975;43(5):

533-539.

49. Downs JB, Douglas ME, Sanfelippo PM, Stanford W,

Hodges MR. Ventilatory pattern, intrapleural pressure,

and cardiac output. Anesth Analg. 1977;56(1):88-96.


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