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High-Frequency

Oscillatory Ventilation
 
Vin K. Gupta, MD
Division of Pediatric Critical Care Medicine
Mercy Children’s Hospital
Toledo, Ohio

Ira M. Cheifetz, MD
Division of Pediatric Critical Care Medicine
Duke Children's Hospital
Durham, North Carolina
Outline
 Review of Acute Lung Injury & Respiratory
Mechanics
 HFOV: A General Overview
 Optimizing Oxygenation
 Optimizing Ventilation
 Routine Management of the Patient on HFOV
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 Ware et al., NEJM, 2000
and edema.
Respiratory Mechanics
 ALI is associated with a decrease
in lung compliance. Volume
 Less volume is delivered for the NORMAL
same pressure delivery during
ALI as compared to normal
conditions.

 Lower and upper inflection points: Acute Lung


Injury
 At the lower end of the curve, the
alveoli are at risk for
derecruitment and collapse.

 At the upper end of the curve, the Pressure


alveoli are at risk of alveolar
overdistension.
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


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


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.
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.
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.


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; 73:123


Pressure-Volume Loop

Froese, CCM, 1997


Open Lung Ventilation Strategy
Zone of Overdistention
Volume

Safe
window

Zone of
Derecruitment
and
atelectasis

Goal is to avoid injury zones


and operate in the safe window Pressure

Froese, CCM, 1997


Outline
 Review of Acute Lung Injury & Respiratory
Mechanics
 HFOV: A General Overview
 Optimizing Oxygenation
 Optimizing Ventilation
 Routine Management of the Patient on HFOV
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
HFOV

CMV
INJURY
Pressure Transmission
 With CMV, the pressures exerted
by the ventilator propagate
through the airway with little HFOV
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.
Gerstmann D.
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
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


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) > 30-35 cm H2O
 FiO2 > 0.60 or the inability to wean
 Mean airway pressure (Paw) > 15 cm H2O
 Peak end expiratory pressure (PEEP) > 10 cm H2O
 Oxygenation index > 13-15

(P aw FO
i 2)

OI = 100

P aO 2
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)
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.
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!!
Outline
 Review of Acute Lung Injury & Respiratory
Mechanics
 HFOV: A General Overview
 Optimizing Oxygenation
 Optimizing Ventilation
 Routine Management of the Patient on HFOV
Variables in Oxygenation
 The two primarily variables that control
oxygenation are:
FiO2

Mean airway pressure (Paw)


Mean Airway Pressure (P aw)
P aw is displayed here
is controlled here

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7.5
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).
Effect of Lung Volume on PVR
Overexpansion

PVR Atelectasis
Total PVR
Small Vessels
Large Vessels
FRC
Lung Volume
Overexpansion
Atelectasis of
of large
PVR is the lowestsmall vessels PVR
at FRC
vessels PVR



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.


Oxygenation – Clinical Tips
 Follow CXR’s 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 < 0.60 within the first
12 hours of HFOV.

 If unable to wean FiO2, consider:


 a recruitment maneuver (sustained inflation)

 increasing the Paw


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.
Outline
 Review of Acute Lung Injury & Respiratory
Mechanics
 HFOV: A General Overview
 Optimizing Oxygenation
 Optimizing Ventilation
 Routine Management of the Patient on HFOV
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
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.
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.
“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
Amplitude Selection
 Start amplitude in the 30’s and adjust until the “wiggle”
extends to the lower level of patient’s 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.
This is displayed as the The power dial
amplitude or P controls the degree of


piston deflection

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7.5
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


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).

Heliox 60
Heliox 40
O 2/N 2

Katz, AJRCCM, 2001


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.
Initial Frequency Settings
 Guidelines for setting the initial frequency.

Patient Weight Hertz


Preterm Neonates 10 to 15
Term Neonates 8 to 10
Children 6 to 8
Adults 5 to 6

 Adjustments in frequency are made in steps of ½ to 1 Hz.


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
Time X
Frequency ()

4 Hz

Lets consider a time interval of X

8 Hz
Time X
Frequency ()

4 Hz

The lower the frequency


setting, the larger the
volume displacement.

8 Hz
Time X
Frequency ()

4 Hz

The higher the


frequency setting, the
smaller the volume
displacement.
8 Hz
Time X
Frequency ()

Therefore, lower
frequencies have a
larger volume
displacement and
improved CO2
elimination.
The frequency is controlled
and read here

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7.5
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.
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.
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.
The inspiratory time is
controlled and read here

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7.5
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.
Outline
 Review of Acute Lung Injury & Respiratory
Mechanics
 HFOV: A General Overview
 Optimizing Oxygenation
 Optimizing Ventilation
 Routine Management of the Patient on HFOV
Sedation/Neuromuscular Blockade
 Transitioning a patient from CMV to HFOV typically
indicates that the patient’s 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.
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.
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
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 CO 2 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.
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


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.
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.
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


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.
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.
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)

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