vin k. gupta, md division of pediatric critical care medicine mercy children ’ s hospital toledo,...

Vin K. Gupta, MDDivision of Pediatric Critical Care Medicine

Mercy Children’s HospitalToledo, Ohio

Ira M. Cheifetz, MDDivision of Pediatric Critical Care Medicine

Duke Children's HospitalDurham, North Carolina

High-Frequency High-Frequency Oscillatory VentilationOscillatory Ventilation

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

Pressure

NORMAL

Acute Lung Injury

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:

BarotraumaVolutraumaAtelectraumaBiotrauma

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

Fu Z, JAP, 1992; 73:123

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.

Pressure-Volume Loop

Froese, CCM, 1997

Open Lung Ventilation Strategy

Volume

Pressure

Zone of Overdistention

Safe window

Zone of Derecruitment and atelectasis

Goal is to avoid injury zones and operate in the safe window

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

INJURY

INJURY

CMVCMV

HFOVHFOV

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.

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.

Gerstmann D.

HFOV

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 F iO 2)

P aO2

100OI =

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)

23 35

33

7.5

P aw is displayed here

Mean Airway Pressure (P aw) is controlled here

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

Lung Volume

PVR

Total PVR

Large VesselsSmall Vessels

Atelectasis

Overexpansion

FRC

PVR is the lowest at FRC Overexpansion ofsmall vessels

PVR

Atelectasis of large

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.

23 35

33

7.5

The power dial controls the degree of piston deflection

This is displayed as the amplitude or P

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).

Katz, AJRCCM, 2001

Heliox 60Heliox 40O 2/

N 2

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.

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

Patient Weight Hertz

Preterm Neonates 10 to 15

Term Neonates 8 to 10

Children 6 to 8

Adults 5 to 6

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

4 Hz

8 Hz

Frequency ()

Lets consider a time interval of X

Time X

4 Hz

8 Hz

The lower the frequency setting, the larger the volume displacement.

Frequency ()

Time X

4 Hz

8 Hz

The higher the frequency setting, the smaller the volume displacement.

Frequency ()

Time X

Therefore, lower frequencies have a larger volume displacement and improved CO2

elimination.

Frequency ()

23 35

33

7.5

The frequency is controlled and read here

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.

23 35

33

7.5

The inspiratory time is controlled and read here

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.: 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)