HFOV

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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
and edema.
Ware et al., NEJM, 2000
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
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 underrecruited 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 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.
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
(Paw  FiO2)
OI =
PaO2
 100
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)
Paw is displayed here
23
Mean Airway Pressure (Paw)
is controlled here
35
33
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
of
Atelectasis
of large
PVR is the lowest small
at FRC
vessels
PVR
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
f x Vt

In CMV, ventilation is defined as:

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
amplitude or P
23
The power dial
controls the degree of
piston deflection
35
33
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
O2/N2
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
Preterm Neonates
Term Neonates
Children
Adults

Hertz
10 to 15
8 to 10
6 to 8
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
Frequency ()
Time X
4 Hz
Lets consider a time interval of X
8 Hz
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.
Time X
The frequency is controlled
and read here
23
35
33
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 itime (max 50%).

Increasing the i-time allows for a larger tidal
volume delivery.
The inspiratory time is
controlled and read here
23
35
33
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 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.
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.: Highfrequency 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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