Vin K. Gupta, MD

1
High-Frequency Oscillatory Ventilation 

• Vin K. Gupta, MD
• Division of Pediatric Critical Care Medicine
• Mercy Childrens Hospital
• Toledo, Ohio
• Ira M. Cheifetz, MD
• Division of Pediatric Critical Care Medicine
• Duke Children's Hospital
• Durham, North Carolina

2
Outline

• Review of Acute Lung Injury Respiratory
  Mechanics
• HFOV A General Overview
• Optimizing Oxygenation
• Optimizing Ventilation
• Routine Management of the Patient on HFOV

3
Acute Lung Injury

• In acute lung injury (ALI) there are 3 regions of
  lung tissue
• Severely diseased regions with a limited ability
  to "safely" recruit.
• Uninvolved regions with normal compliance and
  aeration. Possibility of overdistension with
  increased ventilatory support.
• Intermediate regions with reversible alveolar
  collapse and edema.

Ware et al., NEJM, 2000
4
Respiratory Mechanics

• ALI is associated with a decrease in lung
  compliance.
• Less volume is delivered for the same pressure
  delivery during ALI as compared to normal
  conditions.
• Lower and upper inflection points
• At the lower end of the curve, the alveoli are at
  risk for derecruitment and collapse.
• At the upper end of the curve, the alveoli are at
  risk of alveolar overdistension.

Volume
NORMAL
Acute Lung Injury
Pressure
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Ventilator Associated Lung Injury

• All forms of positive pressure ventilation (PPV)
  can cause ventilator associated lung injury
  (VALI).
• VALI is the result of a combination of the
  following processes
• Barotrauma
• Volutrauma
• Atelectrauma
• Biotrauma

Slutsky, Chest, 1999
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Barotrauma

• High airway pressures during PPV can cause lung
  overdistension with gross tissue injury.
• This injury can allow the transfer of air into
  the interstitial tissues at the proximal airways.
• Clinically, barotrauma presents as pneumothorax,
  pneumomediastinum, pneumopericardium, and
  subcutaneous emphysema.

Slutsky, Chest, 1999
7
Volutrauma

• Lung overdistension can cause diffuse alveolar
  damage at the pulmonary capillary membrane.
• This may result in increased epithelial and
  microvascular permeability, thus, allowing fluid
  filtration into the alveoli (pulmonary edema).
• Excessive end-inspiratory alveolar volumes are
  the major determinant of volutrauma.

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Atelectrauma

• Mechanical ventilation at low end-expiratory
  volumes may be inefficient to maintain the
  alveoli open.
• Repetitive alveolar collapse and reopening of the
  under-recruited alveoli result in atelectrauma.
• The quantitative and qualitative loss of
  surfactant may predispose to atelectrauma.

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Biotrauma

• In addition to the mechanical forms of injury,
  PPV activates an inflammatory reaction that
  perpetuates lung damage.
• Even ARDS from non-primary etiologies will result
  in activation of the inflammatory cascade that
  can potentially worsen lung function.
• This biological form of trauma is known as
  biotrauma.

10
Capillary Leak

• Electron microscopy demonstrates the disruption
  of the alveolar-capillary membrane secondary to
  mechanical ventilation with lung distention.
• Note the leakage of RBCs and other material into
  the alveolar space.

Fu Z, JAP, 1992 73123
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Pressure-Volume Loop
Froese, CCM, 1997
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Open Lung Ventilation Strategy
Goal is to avoid injury zones and operate in the
safe window
Froese, CCM, 1997
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Outline

• Review of Acute Lung Injury Respiratory
  Mechanics
• HFOV A General Overview
• Optimizing Oxygenation
• Optimizing Ventilation
• Routine Management of the Patient on HFOV

14
Pressure and Volume Swings

• During CMV, there are swings between the zones of
  injury from inspiration to expiration.
• During HFOV, the entire cycle operates in the
  safe window and avoids the injury zones.

INJURY
INJURY
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Pressure Transmission

• With CMV, the pressures exerted by the ventilator
  propagate through the airway with little
  dampening.
• With HFOV, there is attenuation of the pressures
  as air moves toward the alveolar level.
• Thus, with CMV the alveoli receive the full
  pressure from the ventilator. Whereas in HFOV,
  there is minimal stretching of the alveoli and,
  therefore, less risk of trauma.

HFOV
Gerstmann D.
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Lung Protective Strategies

• Utilizing HFOV in an open lung strategy provides
  a more effective means to recruit and protect
  acutely injured lungs.
• The ability to recruit and maintain FRC with
  higher mean airway pressures may
• improve lung compliance
• decrease pulmonary vascular resistance
• improve gas exchange
• With attenuation of ?P, there is less trauma to
  the lungs and, therefore, less risk of VALI.
• HFOV improves outcome by ? shear forces
  associated with the cyclic opening of collapsed
  alveoli.

Arnold, PCCM, 2000
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HFOV - General Principles

• A CPAP system with piston displacement of gas
• Active exhalation
• Tidal volume less than anatomic dead space
  (1 to 3 ml/kg)
• Rates of 180 900 breaths per minute
• Lower peak inspiratory pressures for a given mean
  airway pressure as compared to CMV
• Decoupling of oxygenation ventilation

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Indications for HFOV

• Inadequate oxygenation that cannot safely be
  treated without potentially toxic ventilator
  settings and, thus, increased risk of VALI.
• Objectively defined by
• Peak inspiratory pressure (PIP) gt 30-35 cm H2O
• FiO2 gt 0.60 or the inability to wean
• Mean airway pressure (Paw) gt 15 cm H2O
• Peak end expiratory pressure (PEEP) gt 10 cm H2O
• Oxygenation index gt 13-15

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Relative Indications for HFOV(Regardless of
ventilator settings or gas exchange)

• Alveolar hemorrhage (Pappas, Chest, 1996)
• Sickle cell disease in acute chest syndrome
  (Wratney, Resp Care, 2004)
• Large airleak with inability to keep lungs open
  (Clark, CCM, 1986)
• Inadequate alveolar ventilation with respiratory
  acidosis (Arnold, PCCM, 2000)

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Patient Selection

• The clinical goals and guidelines presented are
  for the typical patient with ALI/ARDS.
• The goals may differ for
• Other disease states reactive airway disease,
  acute chest syndrome, flail chest, congenital
  diaphragmatic hernia, sepsis, pulmonary
  hypertension.
• Certain patient groups congenital cardiac
  disease, closed head injury.

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Clinical Goals

• Reasonable oxygenation to limit oxygen toxicity
• SaO2 86 to 92
• PaO2 55 to 90 mm Hg
• Permissive hypercapnea
• Provide just enough ventilatory support to
  maintain normal cellular function.
• Monitor cardiac function, perfusion, lactate, pH
• Allow PaCO2 to rise but keep arterial pH 7.25 to
  7.30. (Derdak, CCM, 2003)
• This strategy helps to minimize
  VALI. (Hickling, CCM, 1998)
• Normal pH, PaCO2, PaO2 are indictors of
  OVERventilation!!

22
Outline

• Review of Acute Lung Injury Respiratory
  Mechanics
• HFOV A General Overview
• Optimizing Oxygenation
• Optimizing Ventilation
• Routine Management of the Patient on HFOV

23
Variables in Oxygenation

• The two primarily variables that control
  oxygenation are
• FiO2
• Mean airway pressure (Paw)

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Mean Airway Pressure (Paw) is controlled here
Paw is displayed here
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Mean Airway Pressure (Paw)

• Use to optimize lung volume and, thus, alveolar
  surface area for gas exchange.
• Utilize Paw to
• recruit atelectatic alveoli
• prevent alveoli from collapsing (derecruitment)
• Although the lung must be recruited, guard
  against overdistension.
• Alveolar atelectasis or overdistension can result
  in ? pulmonary vascular resistance (PVR).

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Effect of Lung Volume on PVR
Overexpansion
Atelectasis
PVR
Total PVR
PVR is the lowest at FRC
Small Vessels
Overexpansion of small vessels ? PVR
Atelectasis of large vessels ? PVR
Large Vessels
FRC
Lung Volume
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Oxygenation Clinical Tips

• Initiate HFOV with
• FiO2 1.0
• Paw 5-8 cm H2O greater than Paw on CMV
• Increase Paw by 1 - 4 cm H2O to achieve optimal
  lung volume.
• Optimal lung volume is determined by
• increase in SaO2 allowing the FiO2 to be weaned
• diaphragm is at ?T9 on chest radiograph
• Maintain the Paw and wean the FiO2 until 0.60.

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Oxygenation Clinical Tips

• Follow CXRs to assess lung expansion.
• If the diaphragm is between 8 and 8½, continue to
  wean the oxygen.
• If the diaphragm is between 9 and 9½, wean the
  Paw by 1 cm H2O.
• You should be able to wean the FiO2 to lt 0.60
  within the first 12 hours of HFOV.
• If unable to wean FiO2, consider
• a recruitment maneuver (sustained inflation)
• increasing the Paw

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Oxygenation Clinical Tips

• Lung perfusion must be matched to ventilation for
  adequate oxygenation (V/Q matching).
• Ensure adequate intravascular volume cardiac
  output.
• The higher intrathoracic pressure may adversely
  affect cardiac preload.
• Consider volume loading (? 5 mL/kg) or initiating
  inotropes.
• Closely monitor hemodynamic status.
• Utilize pulse oximetry and transcutaneous
  monitors to wean FiO2 between blood gas analyses.

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Outline

• Review of Acute Lung Injury Respiratory
  Mechanics
• HFOV A General Overview
• Optimizing Oxygenation
• Optimizing Ventilation
• Routine Management of the Patient on HFOV

31
Ventilation

• The two primarily variables that control
  ventilation are
• Tidal volume (?P or amplitude)
• Controlled by the force with which the
  oscillatory piston moves. (represented as stroke
  volume or ?P)
• Frequency (?)
• Referenced in Hertz (1 Hz 60 breaths/second)
• Range 3 - 15 Hz

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Variables in Ventilation

• In CMV, ventilation is defined as f x Vt
  
• In HFOV, ventilation is defined as f x
  Vt1.5-2.5
• Therefore, changes in Vt delivery have a larger
  effect on ventilation than changes in frequency.

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Amplitude (?P)

• The power control regulates the force and
  distance with which the piston moves from
  baseline.
• The degree of deflection of the piston
  (amplitude) determines the tidal volume.
• This deflection is clinically demonstrated as the
  wiggle seen in the patient.
• The wiggle factor can be utilized in assessing
  the patient.

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Wiggle Factor

• Reassess after positional changes
• If chest oscillation is diminished or absent
  consider
• decreased pulmonary compliance
• ETT disconnect
• ETT obstruction
• severe bronchospasm
• If the chest oscillation is unilateral, consider
• ETT displacement (right mainstem)
• pneumothorax

35
Amplitude Selection

• Start amplitude in the 30s and adjust until the
  wiggle extends to the lower level of patients
  groin.
• Adjust in increments of 3 to 5 cm H2O
• Subjectively follow the wiggle
• Objectively follow transcutaneous CO2 and PaCO2
• Remember, the goal is not to achieve normal
  PaCO2 and pH, but to minimize VALI.

36
This is displayed as the amplitude or ?P
The power dial controls the degree of piston
deflection
37
Resonance Frequency

• There is a resonance frequency of the lungs in
  which optimal ventilation (CO2 removal) occurs.
• Resonance frequency varies based on
• lung size
• the degree of lung injury

Katz, AJRCCM, 2001
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Resonance Frequency

• In this example, 7 Hz represents the resonance
  frequency at which a greater tidal volume
  delivery occurs for the same amplitude (i.e.,
  piston deflection).

Katz, AJRCCM, 2001
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Resonance Frequency

• The resonance frequency depends on
• the amount of functional lung
• the type and extent of the disease state
• the size of the patient
• Therefore, the resonance frequency can vary
  between patients and in the same patient over the
  time.

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Initial Frequency Settings

• Guidelines for setting the initial frequency.
• Adjustments in frequency are made in steps of ½
  to 1 Hz.

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Frequency (?)

• To evaluate the effects of changes in frequency
  with regards to CO2 elimination, let us look at 2
  different frequencies.
• 4 Hz
• 8 Hz

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Frequency (?)
Lets consider a time interval of X
4 Hz
8 Hz
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Frequency (?)
4 Hz
The lower the frequency setting, the larger the
volume displacement.
8 Hz
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Frequency (?)
4 Hz
The higher the frequency setting, the smaller the
volume displacement.
8 Hz
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Frequency (?)
Therefore, lower frequencies have a larger volume
displacement and improved CO2 elimination.
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The frequency is controlled and read here
47
Improving Ventilation

• To improve ventilation first increase the
  amplitude.
• If this does not improve CO2 elimination,
  consider decreasing the frequency.
• Although controversial, some centers consider
  decreasing the frequency by 1 Hz once the
  amplitude is ? 3 times the Paw.

48
Ventilation - Clinical Tips

• With cuffed endotracheal tubes, minimally
  deflating the cuff may improve ventilation.
• Monitor for a loss in Paw with the airleak
  created by deflating the cuff.

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Inspiratory Time

• The initial inspiratory time setting is 33.
• If carbon dioxide elimination is inadequate,
  despite deflating the ETT cuff (or if the patient
  has an uncuffed tube), consider increasing the
  i-time (max 50).
• Increasing the i-time allows for a larger tidal
  volume delivery.

50
The inspiratory time is controlled and read here
51
Improved Ventilation

• If there is appropriate chest wiggle and the
  PaCO2 is too low, consider increasing the
  frequency.
• Once you have improved ventilation or are in the
  weaning phase, do not forget to
• decrease i-time to 33.
• reinflate the ETT cuff (if deflated).
• raise/adjust the frequency as the resonance
  frequency of the lungs changes.
• wean the amplitude.

52
Outline

• Review of Acute Lung Injury Respiratory
  Mechanics
• HFOV A General Overview
• Optimizing Oxygenation
• Optimizing Ventilation
• Routine Management of the Patient on HFOV

53
Sedation/Neuromuscular Blockade

• Transitioning a patient from CMV to HFOV
  typically indicates that the patients
  respiratory distress has worsened.
• To facilitate capturing the patient, additional
  sedation may be required.
• Neuromuscular blockade may be required.
• As the patient improves, discontinue the
  paralysis and wean the sedation as tolerated.

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Auscultation

• Listen to the lung fields to primarily assess the
  presence and symmetry of piston sounds.
• Asymmetry may indicate improper ETT placement,
  pneumothorax, heterogeneous gross lung disease,
  or mucus plugging.
• Pause the piston to perform a cardiac exam and
  assess heart sounds.
• With the piston paused you have placed the
  patient in a CPAP mode and will have maintained
  Paw.

55
Chest Radiographs

• Typically obtain a chest radiograph 1 hour after
  initiating HFOV and then Q12-24 hours.
• Assess
• ETT placement
• Rib expansion (goal is ? 9 ribs)
• Pneumothorax / airleak syndrome
• Change in lung disease

56
Suctioning

• Indications
• Routine suctioning to ensure the ETT remains
  patent
• Frequency of suctioning varies by institution.
• Our policy is every 12 to 24 hours and prn.
• Decreased/absent wiggle
• Possibly from mucus plugs/secretions
• Decrease in SpO2 or transcutaneous O2 level
• Increase in transcutaneous CO2 level
• Suctioning de-recruits lung volume
• May be minimized but not fully eliminated with
  closed suction system.
• May require a sustained inflation recruitment
  maneuver following suctioning.

57
Sustained Inflation (SI)

• A sustained inflation is a lung recruitment
  maneuver.
• There are several ways in which to perform a SI
  maneuver.
• In our institution, the piston is paused (thus
  leaving the patient in CPAP) and the Paw is
  increased by 8-10 cm H2O for 30-60 seconds.
• Once the SI maneuver is completed, the piston is
  restarted.
• Potential complications
• Pneumothorax
• CV compromise / altered hemodynamics

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When To Utilize A SI Maneuver

• When initiating HFOV to recruit lung
• After a disconnect or loss of FRC/Paw
• After suctioning (even with a closed suction
  system)
• Inability to wean FiO2
• When considering increasing Paw
• A recruitment maneuver may recruit lung allowing
  you to maintain the baseline Paw and, thus, not
  increase support.

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Potential Complications of HFOV

• The higher intrathoracic pressures with HFOV may
  decrease RV preload and require volume
  administration inotropic support.
• Pneumothorax
• Migration/displacement of ETT
• Bronchospasm
• Acute airway obstruction from mucus plugging,
  secretions, hemorrhage or clot.

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Summary

• Open the lungs and keep them open
• HFOV improves outcome by ? shear forces
  associated with the cyclic opening of collapsed
  alveoli. (Krishnan, Chest, 2000)
• Minimize ?P (i.e., shear injury) to the lungs by
  minimizing the swings from inspiration to
  expiration.
• Ventilate in the safe window.
• Oxygenation and ventilation are dissociated.
• Adjust Paw independently of ?P

61
Looking towards the future

• A great deal remains unknown about HFOV
• the exact mechanism of gas exchange
• the most effective strategy to manipulate
  ventilator settings
• the safest approach to manipulate ventilator
  settings
• a reliable method to measure tidal volume
• the appropriate use of sedation and neuromuscular
  blockade to optimize patient-ventilator
  interactions
• Additional research in these and other issues
  related to HFOV are necessary to maximize the
  benefit and minimize the potential risks
  associated with HFOV.

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Looking towards the future

• A great deal remains unknown about ARDS in the
  pediatric patient.
• Although there has been a substantial quantity of
  research performed in using various treatment
  options in adults (prone positioning, steroids,
  iNO, tidal volume, etc.), many of these therapies
  have not been evaluated in pediatric patients
  with ARDS.
• Additional research in the pathophysiology of
  pediatric ARDS and various treatment options is
  necessary.

63
References

• Priebe GP, Arnold JH High-frequency oscillatory
  ventilation in pediatric patients. Respir Care
  Clin N Am 2001 7(4)633-645
• Arnold JH, Anas NG, Luckett P, Cheifetz IM, Reyes
  G, Newth CJ, Kocis KC, Heidemann SM, Hanson JH,
  Brogan TV, et al. High-frequency oscillatory
  ventilation in pediatric respiratory failure a
  multicenter experience. Crit Care Med 2000
  28(12)3913-3919
• Arnold JH High-frequency ventilation in the
  pediatric intensive care unit. Pediatr Crit Care
  Med 2000 1(2)93-99
• Slutsky, AS Lung Injury Caused by Mechanical
  Ventilation. Chest 1999 116(1)9S-14S
• dos Santos CC, Slutsky AS Overview of
  high-frequency ventilation modes, clinical
  rationale, and gas transport mechanisms. Respir
  Care Clin N Am 2001 7(4)549-575
• Duke PICU Handbook (revised 2003)
• Duke Ventilator Management Protocol (2004)