High Frequency Oscillatory Ventilation

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Information about High Frequency Oscillatory Ventilation

Published on February 4, 2014

Author: drasimrana

Source: slideshare.net


HFO is a well debated topic but still man ICU physicians and respiratory therapists seem to be afraid of it and avoid this therapy. If in expert hands and utilized judicially it has saved lives and still has a lot of potential in it nit yet explored. Although this presentation is very long but it is drafted by keeping in ind to explain every thing about high frequency oscillatory ventilator to a beginner.

2/4/2014 Muhammad Asim Rana MBBS, MRCP, FCCP, EDIC, SF-CCM Department of Critical Care Medicine King Saud Medical City Riyadh, Saudi Arabia 1

Mechanical ventilation is the cornerstone of supportive care for acute respiratory failure. In most patients, adequate gas exchange can be ensured while more specific treatments are administered. 2/4/2014 2

Conventional Ventilation, its limitations & development of HFV 2/4/2014 3

   High airway pressures, Circulatory depression, and Pulmonary air leaks. 2/4/2014 4

 In patients with acute lung injury (ALI) and ARDS, conventional mechanical ventilation (CV) may cause additional lung injury. 2/4/2014 5

Pressure Volume Curve 2/4/2014 6

Paw = Lung Volume Changing Lung Volume In CV 2/4/2014 7

CT 1 CT 2 CT 3 Paw = CDP Continuous Distending 2/4/2014 Pressure CDP= FRC 8

Optimized Lung Volume “Safe Window”  Overdistension • Edema fluid accumulation • Surfactant degradation • High oxygen exposure • Mechanical disruption Zone of Overdistention Injury  Derecruitment Atelectasis • Repeated closure / reexpansion • Stimulation inflammatory response • Inhibition surfactant • Local hypoxemia • 2/4/2014 Compensatory overexpansion “Safe” Window Volume Zone of Derecruitment and Atelectasis Injury Pressure 9

         An alternate mode of ventilation may be instituted in an attempt to provide adequate gas exchange and limit ventilator-induced lung injury. Approaches used in patients with severe lung injury include: Inverse ratio ventilation Pressure-limited ventilation Airway pressure release ventilation Recruitment maneuvers Prone positioning High frequency ventilation Nitric oxide Extracorporeal CO2 removal and ECMO 2/4/2014 10

 These adverse effects stimulated the development of high-frequency ventilation (HFV). (There was great enthusiasm for HFV during its early development in the 1970s and 1980s). 2/4/2014 11

However, the initial enthusiasm for HFV waned as clinical studies failed to demonstrate important advantages over Conventional Ventilation. 2/4/2014 12

There is now renewed interest in HFV because of increasing evidence that   (1) CV may contribute to lung injury in patients with acute lung injury (ALI) and ARDS (2) modifications of mechanical ventilation techniques may prevent or reduce lung injury and improve clinical outcomes in these patients. 2/4/2014 13

Potential role of HFV Achieving adequate gas exchange while protecting the lung against further injury in patients with ALI/ARDS. TI - Use of ultrahigh frequency ventilation in patients with ARDS. A preliminary report. AU - Gluck E; Heard S; Patel C; Mohr J; Calkins J; Fink MP; Landow L 2/4/2014 SO - Chest 1993 May;103(5):1413-20. 14

Introduction  HFV is a mode of mechanical ventilation that uses rapid respiratory rates (respiratory rate [f] more than four times the normal rate) and small Vts. 2/4/2014 15

Variations of HFV These may be broadly classified as 1. high-frequency positive pressure ventilation (HFPPV), 2. high-frequency jet ventilation (HFJV), and 3. high-frequency oscillation (HFO). 2/4/2014 16

HFPPV   HFPPV was introduced by Oberg and Sjostrand in 1969. HFPPV delivers small Vts (approximately 3 to 4 mL/kg) of conditioned gas at high flow rates (175 to 250 L/min) and frequency (f, 60 to 100 breaths/min). 2/4/2014 17

   The precise Vt is difficult to measure. Expiration is passive and depends on lung and chest wall elastic recoil. Thus, with high f, there is a risk of gas trapping with over distention of some lung regions and adverse circulatory effects. 2/4/2014 18

  Sanders introduced HFJV in 1967 to facilitate gas exchange during rigid bronchoscopy. In HFJV, gas under high pressure (15 to 50 lb per square inch)is introduced through a smallbore cannula or aperture(14 to 18 gauge) into the upper or middle portion of the endotracheal tube. 2/4/2014 HFJV 19

   Pneumatic, fluid, or solenoid valves control the intermittent delivery of the gas jets. Aerosolized saline solution in the inspiratory circuit is used to humidify the inspired air. Some additional gas is entrained during inspiration from a side port in the 2/4/2014 circuit. 20

  This form of HFV generally delivers a Vt of 2 to 5 mL/kg at a f of 100 to 200 breaths/min. The jet pressure (which determines the velocity of air jets) and the duration of the inspiratory jet (and, thus, the inspiratory/expiratory ratio [I/E]) are controlled by the operator. 2/4/2014 21

  Together, the jet velocity and duration determine the volume of entrained gas. Thus, the Vt is directly proportional to the jet pressure and I/E. 2/4/2014 22

  As with HFPPV, expiration is passive. Thus, HFJV may cause air trapping. 2/4/2014 23

High Frequency Oscillation    Lunkenheimer et al introduced HFO in 1972. HFO uses reciprocating pumps or diaphragms. Thus, in contrast to HFPPV and HFJV, both expiration and inspiration are active processes during HFO. 2/4/2014 24

  HFO Vts are approximately 1 to 3 mL/kg at fs up to 2,400 breaths/min. The operator sets the f, the I/E (typically approximately 1:2), driving pressure, and mean airway pressure (MAP). 2/4/2014 25

   The oscillatory Vts are directly related to driving pressures. In contrast, Vts are inversely related to frequency. The inspiratory bias flow of air into the airway circuit is adjusted to achieve the desired MAP 2/4/2014 26

2/4/2014 27

Frequency controls the time allowed (distance) for the piston to move. Therefore, the lower the frequency , the greater the volume displaced, and the higher the frequency , the smaller the volume displaced. 2/4/2014 28

HFOV Principle: I + + + + + Amplitude Delta P = Tv = Ventilation CDP=FRC= Oxygenation E 2/4/2014 - - - - HFOV = CPAP with a wiggle ! - 29

Pressure transmission CMV / HFOV   Distal amplitude measurements with alveolar capsules in animals, demonstrate it to be greatly reduced or “attenuated” as the pressure traverses through the airways. Due to the attenuation of the pressure wave, by the time it reaches the alveolar region, it is reduced down to .1 - 5 cmH2O. 2/4/2014 Gerstman et al 30

Pressure transmission HFOV proximal trachea alveoli P 2/4/2014 31 T

Advantages of HFO 1. 2. 3. 4. There is no gas entrainment or decompression of gas jets in the airway, allowing better humidification and warming of inspired air. The risks of airway obstruction from desiccated airway secretions is lower. In addition, active expiration permits better control of lung volumes than with HFPPV and HFJV, decreasing the risk of air trapping, overdistention of airspaces, and circulatory depression. Lower I/Es (1:2 or 1:3) reduce the risk of air trapping. 2/4/2014 32

Selected Features of CV & HFV 2/4/2014 33

Gas Transport During HFV 2/4/2014 34

1.Direct Bulk Flow  Some alveoli situated in the proximal tracheobronchial tree receive a direct flow of inspired air. This leads to gas exchange by traditional mechanisms of convective or bulk flow. 2/4/2014 35

2.Longitudinal (Taylor) Dispersion  Turbulent eddies and secondary swirling motions occur when convective flow is superimposed on diffusion. Some fresh gas may mix with gas from alveoli, increasing the amount of gas exchange that would occur from simple bulk flow. 2/4/2014 36

3.Pendeluft  Units can mutually exchange gas, an effect known as pendeluft. By way of this mechanism even very small fresh-gas volumes can reach a large number of alveoli and regions 2/4/2014 37

2/4/2014 38

4.Asymmetric Velocity Profiles    The velocity profile of air moving through an airway under laminar flow conditions is parabolic. Air closest to the tracheobronchial wall has a lower velocity than air in the center of the airway lumen. This parabolic velocity profile is usually more pronounced during the inspiratory phase of respiration because of differences in flow rates. 2/4/2014 39

 With repeated respiratory cycles, gas in the center of the airway lumen advances further into the lung while gas on the margin (close to the airway wall) moves out toward the mouth. 2/4/2014 40

  During inspiration, the high frequency pulse creates a bullet shaped profile with the central molecules moving further down the air way than those molecules found on the periphery of the airway. On exhalation, the velocity profile is blunted so that at the completion of each return , the central molecules remain further down the airway and the peripheral molecules move towards the mouth of the airway. 2/4/2014 41

5.Cardiogenic Mixing  Mechanical agitation from the contracting heart contributes to gas mixing, especially in peripheral lung units in close proximity to the heart. 2/4/2014 42

6.Molecular Diffusion  As in other modes of ventilation, this mechanism may play an important role in mixing of air in the smallest bronchioles and alveoli, near the alveolocapillary membranes. 2/4/2014 43

ALI/ARDS 2/4/2014 44

2/4/2014 45

 Chest Radiographs & CT Images 2/4/2014 46

  Patients with ALI/ARDS frequently develop acute respiratory failure. Physiologic dead space typically is also elevated, which increases the minute ventilation required to maintain normal arterial Paco2 and pH. TI - High-frequency percussive ventilation improves oxygenation in trauma patients with acute respiratory distress syndrome: a retrospective review.AU - Eastman A; Holland D; Higgins J; Smith B; Delagarza J; Olson C; Brakenridge S; Foteh K; Friese RSO - Am J Surg. 2006 Aug;192(2):191-5. 2/4/2014 47

Our Rescue here is Mechanical Ventilation BUT IT IS NOT EASY 2/4/2014 48

Ventilator Associated Lung Injury  Uneven distribution of Tidal Volumes  Pro inflammatory mediators 2/4/2014 49

Mechanisms of VALI in ALI/ARDS 1. 2. 3. Ventilation of lung regions with higher compliance may be injured by excessive regional end inspiratory lung volumes (EILVs). Injury may occur in small bronchioles when they snap open during inspiration and close during expiration. Pulmonary parenchyma at the margins between atelectatic and aerated units may be injured by excessive stress from the interdependent connections between adjacent units. 2/4/2014 50

 These last two mechanisms are frequently described with the term shear forces and may be important mechanisms of lung injury when ventilation occurs with relatively low end expiratory lung volumes (EELVs) in patients with ALI/ARDS. 2/4/2014 51

Injury From Excessive EILVs   The lungs of patients with ALI/ARDS are susceptible to excessive regional EILV and over distention injury High inspiratory airway pressures (peak and plateau). 2/4/2014 52

Volutrauma   Excessive lung stretch, rather than pressure, is more likely to be the injurious force. Thus, there is increasing use of the term volutrauma to refer to the stretch-induced injury of excessive inspiratory gas volume. 2/4/2014 53

Injury From Ventilation at Low EELVs  Positive end-expiratory pressure (PEEP) has lung protective effects during mechanical ventilation in isolated lungs, and in intact and open-chest animals. 2/4/2014 54

    Effect of PEEP on edema with large lung volumes Injury caused by ventilation with large Vt and low PEEP. Effects of smaller Vts and higher PEEPs despite similar EILVs. The effect of end-expiratory atelectasis on lung injury. 2/4/2014 55

PEEP Good Or Bad 2/4/2014 56

   These and other studies provide convincing evidence that PEEP has lung protective effects during mechanical ventilation. However, PEEP also can contribute to lung injury by raising EILV unless Vt is simultaneously reduced. Moreover, PEEP may cause circulatory depression from increased pulmonary vascular resistance and decreased venous return. 2/4/2014 57

CV-Based Lung Protective Strategies CV strategies designed to protect the lung from VALI have been tested in several clinical trials. 2/4/2014 58

Studies With Reduced EILV In two case series of patients with severe ARDS (a total of approximately 100 patients), ventilation with small Vts (reduced EILVs) was associated with mortality rates that were substantially lower than rates predicted from the patients’ acute physiology and chronic health evaluation (APACHE) II scores. 2/4/2014 Ventilation with lower tidal volumes as compared with 59 traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301.

In contrast   A large multicenter trial with 861 patients with ALI/ARDS found substantial improvements in clinical outcomes in the small Vt group. The mortality rate prior to discharge home with unassisted breathing was significantly reduced (31% vs 40%, respectively; p , 0.01) among patients randomized to the small Vt strategy. 2/4/2014 60

Studies With Reduced EILV and Increased EELV A clinical trial in 53 patients with severe ARDS compared a traditional CV approach with an approach designed to protect the lung from VALI resulting from both excessive EILV and inadequate EELV. 2/4/2014 61

In the lung-protection group, pressure limited modes were used with Vts # 6 mL/kg and peak inspiratory pressures 40 cm H20 to reduce EILV. Increased EELV was achieved, raising PEEP. Frequent recruitment maneuvers were introduced to further increase EELV, and additional measures were taken to avoid undesirable collapse or derecruitment of some lung regions. 2/4/2014 62

The lung protection approach was associated with an improved 28-day survival rate and weaning rate. In hospital mortality rate was also reduced 2/4/2014 Brower RG, Shanholtz CB, Fessler HE, et al. Prospective randomized, controlled clinical trial comparing traditional vs reduced tidal volume ventilation in ARDS patients. Crit CareMed 1999; 27:1492–1498 63

Summary Lung Protective Modes of CV The body of experimental evidence strongly suggests that a lung protective strategy with smaller EILV and higher EELV will reduce VALI and improve outcomes in patients with ALI/ARDS. 2/4/2014 64

Limitations Increasing EELV (with higher PEEPs), especially when it is used in combination with lower EILVs (smaller Vts) during CV may cause  hypoventilation  respiratory acidosis  Dyspnea  circulatory depression  increased cerebral blood flow & risk for intracranial hypertension  increase the requirements for heavy sedation and neuromuscular blockade. 2/4/2014 65

Rationale for HFV-Based Lung Protective Strategies 2/4/2014 66

HFV Advantages over CV 1. HFV uses very small VTs. This allows the use of higher EELVs to achieve greater levels of lung recruitment while avoiding injury from excessive EILV. 2. Respiratory rates with HFV are much higher than with CV. This allows the maintenance of normal or near-normal Paco2 levels, even with very small Vts. - High-frequency percussive ventilation improves TI 2/4/2014 oxygenation in trauma patients with acute respiratory distress syndrome: a retrospective review.AU - Eastman A; Holland D; 67 Higgins J; Smith B; Delagarza J; Olson C; Brakenridge S; Foteh K; Friese RSO - Am J Surg. 2006 Aug;192(2):191-5.

HFOV Principle Pressure curves CMV / HFOV 2/4/2014 68

Adults Studies HFJV was compared to CV in a randomized trial of 309 oncology patients with body weight > 20 kg and respiratory failure requiring mechanical ventilation In another study, 113 surgical ICU patients at risk for ARDS were randomized to highfrequency percussive ventilation (HFPV) or CV In a 1997 case series, 17 medical and surgical patients (age range, 17 to 83 years) with severe ARDS 2/4/2014 69

Conclusion 2/4/2014 70

Small Vt ventilation to reduce EILV during CV recently has shown to improve mortality when compared to a more traditional Vt approach. There is also abundant evidence in experimental animals and, more recently, in humans to suggest that there are lung protective effects with higher EELV. HFV, especially HFO, offers the best opportunity to achieve greater lung recruitment without overdistention while maintaining normal or near-normal acidbase parameters. 2/4/2014 71

Starting on HFO TI - A protocol for high-frequency oscillatory ventilation in adults: results from a roundtable discussion. AU - Fessler HE; Derdak S; Ferguson ND; Hager DN; Kacmarek RM; Thompson BT; Brower RG 2/4/2014 SO - Crit Care Med. 2007 Jul;35(7):1649-54. 72

2/4/2014 73

Diagrammatic Representation 2/4/2014 74

SensorMedics 3100B       Electrically powered, electronically controlled piston-diaphragm oscillator Paw of 5 - 55 cmH2O Pressure Amplitude from 8 - 130 cmH2O Frequency of 3 - 15 Hz % Inspiratory Time 30% - 50% Flow rates from 0 - 60 LPM 2/4/2014 75

Indications     Diffuse alveolar disease associated with decreased lung compliance, hypoxemia & Oxygen index > 30 Oxygen index=FiO2*Paw/PaO2*100 Pulmonary barotrauma with air leak syndrome CXR: Pneumothorax Pneumomediastinum pneumoperitoneum 2/4/2014 76

Contraindications   Heterogenous lung disease Increased expiratory resistance 2/4/2014 77

Initiation    1. Connect patient to HFO circuit 2. FiO2 100% 3. Perform recruitment maneuvers TI - Tidal volume delivery during high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. AU - Hager DN; Fessler HE; Kaczka DW; Shanholtz CB; Fuld MK; Simon BA; Brower RG SO - Crit Care Med. 2007 Jun;35(6):1522-9. 2/4/2014 78

Initial Settings       1. 2. 3. 4. FiO2 100% I:E 1:2 ( Inspiratory Time 33%) Bias Flow 40 liters/min Pressure amplitude (∆P) 90cmH2O 5. mPaw 30 cm of H2O 6. frequency is determined by arterial pH immediately prior to HFO 2/4/2014 79

pH & frequency     <7.10 7.10-7.19 7.20-7.35 >7.35 2/4/2014 3-5Hz 4Hz 5Hz 6Hz 80

Oxygenation       Target SpO2 88-93% & PaO2 55-80mmHg After initial RM decrease FiO2 in 0.05-0.1 decrements Q2-5 minutes to target SpO2 8893 If resultant FiO2 is <0.60, adjust mPaw according to the following chart but if SpO2 falls and you have to increase FiO2 above 0.60: Perform a 2nd RM Reinitiate HFO with mPaw 34cmH2O Follow the chart again 2/4/2014 81

Algorithm to follow Step 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 FiO2 0.4 0.4 0.4 0.4 0.4 0.4 0.5 0.6 0.6 0.6 0.7 0.8 0.9 1.0 1.0 1.0 mPaw 20 22 24 26 28 30 30 30 32 34 34 34 34 34 36 38   Fluctuation of 5 cm of H2O around set mPaw allowable unless oxygenation or ventilation is compromised; otherwise increase sedation. Precede each increase in mPaw by a RM. Physician may discontinue these routine RMs at their discretion after 48 hours in study. Do not decrease mPaw more than 2 cm H2O Q 2Hrs 2/4/2014 82

If patient develops hypotension during mPaw titration, stay at lower possible mPaw 1. 2. 3. 4. 5. Reduce mPaw to 30 cm 0f H2O or most recently tolerated, whichever is lower. Ensure your patient is adequately filled. If patient remains hypotensive despite of sufficient preload start pressors. If lungs appear over distended on CXR and/or patient is unresponsive to increase in mPaw , target a lower mPaw. if FiO2 is > 0.70 for > 2 hrs & intravascular volume is optimized try a lower mPaw. 2/4/2014 83

Recruitment Maneuvers TI - Combining high-frequency oscillatory ventilation and recruitment maneuvers in adults with early acute respiratory distress syndrome: the Treatment with Oscillation and an Open Lung Strategy (TOOLS) Trial pilot study.AU - Ferguson ND; Chiche JD; Kacmarek RM; Hallett DC; Mehta S; Findlay GP; Granton JT; Slutsky AS; Stewart TESO 84 - Crit2/4/2014 Med. 2005 Mar;33(3):479-86. Care

2/4/2014 85

Conventional Ventilation 1. 2. 3. 4. 5. 6. 7. 8. 2/4/2014 9. Increase FiO2 to 1.0 Set pressure alarm limit to 50 cm H2O. Set apnea alarm to 60 seconds. Change to CPAP/PS mode. Assure pressure support is set at “0” & tube compensation is “off” ( tube compensation should always be off for HFO patients). Increase PEEP to 40 & maintain inflation for 40 seconds. Lower PEEP to previous set level. Resume previous set mode & reset alarm limits. Lower FiO2 to previous level. 86

When to perform a RM on HFO    On initiation of HFO Immediately preceding any increase in mPAW dictated by the mPAW/FiO2 chart; after day 2 this is optional at the discretion of the attending physician If a persistent desaturation (SpO2 <88% lasting more than 15 minutes) occurs following an event likely to have caused derecruitment (e.g. suctioning, accidental ventilator disconnection, patient repositioning) ; after day 2 this is optional at the discretion of the attending physician 2/4/2014 87

Recruitment Maneuvers for HFO 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Increase FiO2 to 1.0. Set high pressure alarm to 55 cm H2O. Pause the oscillating membrane (∆ P=0) Eliminate a cuff leak, if present. Slowly raise mPaw to 40 cm H2O over 10 seconds. Maintain mPaw = 40 cm H2O for 40 seconds. Slowly lower mPaw over 10 seconds,to set level prior to RM if RM was conducted for disconnect or derecruitment. Adjust level higher to previous if RM performed for persistent hypoxia. Resume oscillation & reset alarms. Lower the FiO2. 2/4/2014 88

Ventilation    Goal pH 7.25-7.35 at highest possible frequency To minimize Vt, maximize frequency Adjust frequency rather than ∆ P 90 cm H2O to control pH. 2/4/2014 89

pH> 7.35    Increase f by 1 Hz Q 30-60 min to pH goal or F=10 Hz. Decrease delta P from 90 cm only if f=10 Hz & pH > 7.35 without cuff leak. If these criteria are met , Decrease delta p by 10 cm H2O Q 30-60 min to reach pH goal. 2/4/2014 90

pH 7.25 -7.35  Use highest possible frequency within this goal range. 2/4/2014 91

pH 7.15 -7.24  Decrease f by 1 Hz Q 30-60 to reach pH goal or f=4 2/4/2014 92

pH< 7.15   Decrease f by 1 Hz Q 30-60 min to pH goal or f=3. Consider IV bicarb. 2/4/2014 93

pH <7.0   Ensure paralysis. If pH remains low for an hour other rescue measure should be sought. 2/4/2014 94

Weaning  Consider Conventional Ventilation FiO2<0.40 Amplitude<25 cmH2O Frequency 10-15 Hz Paw<20 cmH2O Ti: 33% 2/4/2014 95

Important Considerations       CXRs Piston centering Sedation & paralysis Patient & Circuit positioning Air way patency Recruitment maneuvers after suction 2/4/2014 96

2/4/2014 97

References 2/4/2014 98

    Standiford, TJ, Morganroth, ML. High-frequency ventilation. Chest 1989; 96:1380. Gluck, E, Heard, S, Patel, C, et al. Use of ultrahigh frequency ventilation in patients with ARDS: A preliminary report. Chest 1993; 103:1413. Fessler, HE, Derdak, S, Ferguson, ND, et al. A protocol for high-frequency oscillatory ventilation in adults: results from a roundtable discussion. Crit Care Med 2007; 35:1649. Hager, DN, Fessler, HE, Kaczka, DW, et al. Tidal volume delivery during high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Crit Care Med 2007; 35:1522. 2/4/2014 99

   Salim, A, Martin, M. High-frequency percussive ventilation. Crit Care Med 2005; 33:S241. Carlon, GC, Ray, C, Klain, M, et al. Highfrequency positive pressure ventilation in management of a patient with bronchopleural fistula. Anesthesiology 1980; 52:160. Bishop, MJ, Benson, MS, Sato, P, Pierson, DJ. Comparison of high-frequency jet ventilation with conventional mechanical ventilation for bronchopleural fistula. Anesth Analg 1987; 66:833. 2/4/2014 100

    Eastman, A, Holland, D, Higgins, J, et al. Highfrequency percussive ventilation improves oxygenation in trauma patients with acute respiratory distress syndrome: a retrospective review. Am J Surg 2006; 192:191. Mehta, S, Granton, J, MacDonald, RJ, et al. Highfrequency oscillatory ventilation in adults: the Toronto experience. Chest 2004; 126:518. David, M, Weiler, N, Heinrichs, W, et al. Highfrequency oscillatory ventilation in adult acute respiratory distress syndrome. Intensive Care Med 2003; 29:1656. Carlon, GC, Howland, WS, Ray, C, et al. Highfrequency jet ventilation: A prospective randomized evaluation. Chest 1983; 84:551. 2/4/2014 101

Derdak, S, Mehta, S, Stewart, TE, et al. Highfrequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med 2002; 166:801.  Bollen, CW, van Well, GT, Sherry, T, et al. High frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial [ISRCTN24242669]. Crit Care 2005; 9:R430.  Mentzelopoulos, SD, Roussos, C, Koutsoukou, A, et al. Acute effects of combined high-frequency oscillation and tracheal gas insufflation in severe acute respiratory distress syndrome. Crit Care Med 2007; 35:1500.  Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress 2/4/2014 102 syndrome. N Engl J Med 2000; 342:1301. 

Mehta, S, MacDonald, R, Hallett, DC, et al. Acute oxygenation response to inhaled nitric oxide when combined with high-frequency oscillatory ventilation in adults with acute respiratory distress syndrome. Crit Care Med 2003; 31:383.  Ferguson, ND, Chiche, JD, Kacmarek, RM, et al. Combining high-frequency oscillatory ventilation and recruitment 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; 33:479.  Demory, D, Michelet, P, Arnal, JM, et al. Highfrequency oscillatory ventilation following prone positioning prevents a further impairment in oxygenation. Crit Care Med 2007; 35:106.  Bollen, CW, Uiterwaal, CS, van Vught, AJ. Systematic review of determinants of mortality in high frequency oscillatory ventilation in acute respiratory distress syndrome. Crit Care 2006; 103 2/4/2014 10:R34. 

    Fessler, HE, Hager, DN, Brower, RG. Feasibility of very high frequency ventilation in adults with acute respiratory distress syndrome. Crit Care Med 2008; 36:1043. Reper, P, Wibaux, O, Van Laeke, P, et al. High frequency percussive ventilation and conventional ventilation after smoke inhalation: a randomised study. Burns 2002; 28:503. Hurst, JM, Branson, RD, DeHaven, CB. The role of high-frequency ventilation in post-traumatic respiratory insufficiency. J Trauma 1987; 27:236. Angus, DC, Lidsky, NM, Dotterweich, LM, et al. The influence of high-frequency jet ventilation with varying cardiac-cycle specific synchronization on cardiac output in ARDS. Chest 1997; 112:1600. 2/4/2014 104

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