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Dr.Muhammad Asim Rana

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Title: Dr.Muhammad Asim Rana


1
High Frequency Ventilation
Dr.Asim Rana
Dr.Muhammad Asim Rana
2
  • 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.

3
Conventional Ventilation, its limitations
development of HFV
4
  • High airway pressures,
  • Circulatory depression, and
  • Pulmonary air leaks.

5
  • In patients with acute lung injury (ALI) and
    ARDS, conventional mechanical ventilation (CV)
    may cause additional lung injury.

6
Pressure Volume Curve
7
Changing Lung Volume In CV
Paw Lung Volume
8
CT 2
CT 1
CT 3
Paw CDP
CDP FRC
Continuous Distending Pressure
9
Optimized Lung Volume Safe Window
  • Overdistension
  • Edema fluid accumulation
  • Surfactant degradation
  • High oxygen exposure
  • Mechanical disruption
  • Derecruitment Atelectasis
  • Repeated closure / re-expansion
  • Stimulation inflammatory response
  • Inhibition surfactant
  • Local hypoxemia
  • Compensatory overexpansion

Zone of Overdistention
Injury
Safe Window
Zone of Derecruitment and Atelectasis
Volume
Injury
Pressure
10
  • 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

11
  • 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).

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

13
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.

14
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 SO - Chest 1993 May103(5)1
413-20.
15
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.

16
Variations of HFV
  • These may be broadly classified as
  • high-frequency positive pressure ventilation
    (HFPPV),
  • high-frequency jet ventilation (HFJV), and
  • high-frequency oscillation (HFO).

17
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).

18
  • 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.

19
HFJV
  • 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 small-bore
    cannula or aperture(14 to 18 gauge) into the
    upper or middle portion of the endotracheal tube.

20
  • 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 circuit.

21
  • 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.

22
  • 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.

23
  • As with HFPPV, expiration is passive.
  • Thus, HFJV may cause air trapping.

24
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.

25
  • 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 12), driving pressure, and mean
    airway pressure (MAP).

26
  • 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

27
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28
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.
29
HFOV Principle





I
Amplitude Delta P Tv Ventilation
CDPFRC Oxygenation
-
-
-
-
-
E
HFOV CPAP with a wiggle !
30
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.

Gerstman et al
31
Pressure transmission HFOV
P
T
32
Advantages of HFO
  1. There is no gas entrainment or decompression of
    gas jets in the airway, allowing better
    humidification and warming of inspired air.
  2. The risks of airway obstruction from desiccated
    airway secretions is lower.
  3. 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.
  4. Lower I/Es (12 or 13) reduce the risk of air
    trapping.

33
Selected Features of CV HFV
34
Gas Transport During HFV
35
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.

36
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.

37
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

38
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39
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.

40
  • 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.

41
  • 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.

42
5.Cardiogenic Mixing
  • Mechanical agitation from the contracting heart
    contributes to gas mixing, especially in
    peripheral lung units in close proximity to the
    heart.

43
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.

44
ALI/ARDS
45
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46
  • Chest Radiographs CT Images

47
  • 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 Aug192(2)191-5.
48
Our Rescue here is Mechanical Ventilation
  • BUT IT IS NOT EASY

49
Ventilator Associated Lung Injury
  • Uneven distribution of Tidal Volumes
  • Pro inflammatory mediators

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

51
  • 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.

52
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).

53
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.

54
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.

55
  • 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.

56
PEEP Good Or Bad
57
  • 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.

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

59
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.

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 3421301.
60
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.

61
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.

62
  • 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.

63
  • The lung protection approach was associated with
    an improved 28-day survival rate and weaning
    rate.
  • In hospital mortality rate was also reduced

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
2714921498
64
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.

65
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.

66
Rationale for HFV-Based Lung ProtectiveStrategies
67
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.

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 Aug192(2)191-5.
68
HFOV PrinciplePressure curves CMV / HFOV
Injury
Injury
69
Adults Studies
  • HFJV was compared to CV in a randomized trial of
    309 oncology patients with body weight gt 20 kg
    and respiratory failure requiring mechanical
    ventilation
  • In another study, 113 surgical ICU patients at
    risk for ARDS were randomized to high-frequency
    percussive ventilation (HFPV) or CV
  • In a 1997 case series, 17 medical and surgical
    patients (age range, 17 to 83 years) with severe
    ARDS

70
Conclusion
71
  • 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 acid-base parameters.

72
Starting on HFO
TI - A protocol for high-frequency oscillatory
ventilation in adults results from a roundtable
discussion. AU - Fessler HE Derdak S Ferguson N
D Hager DN Kacmarek RM Thompson BT Brower RG
SO - Crit Care Med. 2007 Jul35(7)1649-54.
73
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74
Diagrammatic Representation
75
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

76
Indications
  • Diffuse alveolar disease associated with
    decreased lung compliance, hypoxemia Oxygen
    index gt 30
  • Oxygen indexFiO2Paw/PaO2100
  • Pulmonary barotrauma with air leak syndrome
  • CXR Pneumothorax
  • Pneumomediastinum
  • pneumoperitoneum

77
Contraindications
  • Heterogenous lung disease
  • Increased expiratory resistance

78
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 Jun35(6)1522-9.
79
Initial Settings
  • 1. FiO2 100
  • 2. IE 12 ( Inspiratory Time 33)
  • 3. Bias Flow 40 liters/min
  • 4. Pressure amplitude (?P)
  • 90cmH2O
  • 5. mPaw 30 cm of H2O
  • 6. frequency is determined by arterial pH
    immediately prior to HFO

80
pH frequency
  • lt7.10 3-5Hz
  • 7.10-7.19 4Hz
  • 7.20-7.35 5Hz
  • gt7.35 6Hz

81
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 88-93
  • If resultant FiO2 is lt0.60, 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

82
Algorithm to follow
16 15 14 13 12 11 10 9 8 7 6 5 4 3 2 1 Step
1.0 1.0 1.0 0.9 0.8 0.7 0.6 0.6 0.6 0.5 0.4 0.4 0.4 0.4 0.4 0.4 FiO2
38 36 34 34 34 34 34 32 30 30 30 28 26 24 22 20 mPaw
  • 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

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

84
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
- Crit Care Med. 2005 Mar33(3)479-86.
85
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86
Conventional Ventilation
  1. Increase FiO2 to 1.0
  2. Set pressure alarm limit to 50 cm H2O.
  3. Set apnea alarm to 60 seconds.
  4. Change to CPAP/PS mode.
  5. Assure pressure support is set at 0 tube
    compensation is off ( tube compensation should
    always be off for HFO patients).
  6. Increase PEEP to 40 maintain inflation for 40
    seconds.
  7. Lower PEEP to previous set level.
  8. Resume previous set mode reset alarm limits.
  9. Lower FiO2 to previous level.

87
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 lt88 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

88
Recruitment Maneuvers for HFO
  1. Increase FiO2 to 1.0.
  2. Set high pressure alarm to 55 cm H2O.
  3. Pause the oscillating membrane (? P0)
  4. Eliminate a cuff leak, if present.
  5. Slowly raise mPaw to 40 cm H2O over 10 seconds.
  6. Maintain mPaw 40 cm H2O for 40 seconds.
  7. Slowly lower mPaw over 10 seconds,to set level
    prior to RM if RM was conducted for disconnect
    or derecruitment.
  8. Adjust level higher to previous if RM performed
    for persistent hypoxia.
  9. Resume oscillation reset alarms.
  10. Lower the FiO2.

89
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.

90
pHgt 7.35
  • Increase f by 1 Hz Q 30-60 min to pH goal or F10
    Hz.
  • Decrease delta P from 90 cm only if f10 Hz pH
    gt 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.

91
pH 7.25 -7.35
  • Use highest possible frequency within this goal
    range.

92
pH 7.15 -7.24
  • Decrease f by 1 Hz Q 30-60 to reach pH goal or
    f4

93
pHlt 7.15
  • Decrease f by 1 Hz Q 30-60 min to pH goal or f3.
  • Consider IV bicarb.

94
pH lt7.0
  • Ensure paralysis.
  • If pH remains low for an hour other rescue
    measure should be sought.

95
Weaning
  • Consider Conventional Ventilation
  • FiO2lt0.40
  • Amplitudelt25 cmH2O
  • Frequency 10-15 Hz
  • Pawlt20 cmH2O
  • Ti 33

96
Important Considerations
  • CXRs
  • Piston centering
  • Sedation paralysis
  • Patient Circuit positioning
  • Air way patency
  • Recruitment maneuvers after suction

97
Enough???
98
References
99
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    ventilation. Chest 1989 961380.
  • Gluck, E, Heard, S, Patel, C, et al. Use of
    ultrahigh frequency ventilation in patients with
    ARDS A preliminary report. Chest 1993 1031413.
  • 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 351649.
  • 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 351522.

100
  • Salim, A, Martin, M. High-frequency percussive
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    High-frequency positive pressure ventilation in
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    fistula. Anesthesiology 1980 52160.
  • Bishop, MJ, Benson, MS, Sato, P, Pierson, DJ.
    Comparison of high-frequency jet ventilation with
    conventional mechanical ventilation for
    bronchopleural fistula. Anesth Analg 1987
    66833.

101
  • Eastman, A, Holland, D, Higgins, J, et al.
    High-frequency percussive ventilation improves
    oxygenation in trauma patients with acute
    respiratory distress syndrome a retrospective
    review. Am J Surg 2006 192191.
  • Mehta, S, Granton, J, MacDonald, RJ, et al.
    High-frequency oscillatory ventilation in adults
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    acute respiratory distress syndrome. Intensive
    Care Med 2003 291656.
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    High-frequency jet ventilation A prospective
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102
  • Derdak, S, Mehta, S, Stewart, TE, et al.
    High-frequency oscillatory ventilation for acute
    respiratory distress syndrome in adults a
    randomized, controlled trial. Am J Respir Crit
    Care Med 2002 166801.
  • 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 9R430.
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    al. Acute effects of combined high-frequency
    oscillation and tracheal gas insufflation in
    severe acute respiratory distress syndrome. Crit
    Care Med 2007 351500.
  • 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 3421301.

103
  • 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 31383.
  • 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 33479.
  • Demory, D, Michelet, P, Arnal, JM, et al.
    High-frequency oscillatory ventilation following
    prone positioning prevents a further impairment
    in oxygenation. Crit Care Med 2007 35106.
  • 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
    10R34.

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