High Frequency Oscillatory Ventilation (HFOV)

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Introduction and Definition

High frequency ventilation (HFV) is a specialized form of mechanical ventilation support that generates high breathing frequencies or respiratory rates, usually greater than 300 breaths/minute in the pediatric age group.
This rapid respiratory rate leads to the delivery of tidal volumes that are less than the anatomical dead space (typically 1.5-2 mL/kg) along with minimal phasic airway pressure swings.
Animal studies have demonstrated that there is a significant dampening or filtering effect of the peak-to-trough pressure swings when moving down from the proximal airway to the level of the alveolus.
This physiological dampening occurs due to the mitigation of pressure swings first at the level of the endotracheal tube and subsequently at the branching generations of the tracheobronchial tree.
This principle is in stark contrast to Conventional Mechanical Ventilation (CMV), where the pressure attained proximally is similar to that achieved at the level of the alveolus.
In HFOV, the mean airway pressure (mPaw) is set at the ventilator, and minimal phasic pressure swings occur around this baseline, keeping a stable tidal volume and mitigating alveolar cyclical collapse and reopening.
With its near dead-space tidal volumes and theoretical ability to ventilate in the safe zone (between the upper and lower inflection points) of a volume-pressure relationship, HFOV qualifies as a lung-protective form of ventilation.

Physiology and Gas Exchange Mechanisms

In conventional ventilation, Alveolar Ventilation is mathematically defined as $T i d a l v o l u m e (V_{T}) \times F r e q u e n c y (ν)$ .
Conversely, in High Frequency Ventilation, Alveolar Ventilation is mathematically defined as $[T i d a l v o l u m e (V_{T})]^{2} \times F r e q u e n c y (ν)$ .
Because of this squared relationship, even a small change in tidal volume during high frequency ventilation may lead to significant changes in minute ventilation.
The optimal frequency on HFOV is often described as the corner frequency ( $F c$ ), at which optimal gas exchange occurs in combination with the least injurious pressures.
Corner frequency is defined by the equation $F c = 1 / (2 π R C)$ , where $R$ is resistance and $C$ is compliance.
The corner frequency is altered by the underlying lung diseases, notably increasing in lung pathologies with short time constants and low compliance, such as Pediatric Acute Respiratory Distress Syndrome (PARDS).
During HFOV, the oscillations are produced by a piston or micro-processor flow controller at a selected rate and displacement.
A continuous bias flow of oxygenated, humidified gas is passed in front of an oscillating membrane, which actively pushes and pulls the gas into and out of the patient.
This active expiration is an attribute entirely unique to HFOV among high-frequency modes.
Gas exchange during HFOV is proposed to occur via six specific mechanisms:
- Taylor dispersion: The diffusion of high-velocity central gases to the smaller margins of the airway.
- Convective dispersion: Asymmetry between inspiratory and expiratory velocity profiles, leading to fresh gas movement more distally in the lungs.
- Cardiogenic mixing: The beating of the heart contributes to a movement of gas in the pericardial regions of the lungs, promoting gas mixing.
- Molecular diffusion: The movement of molecules from higher concentration to lower concentration within small spaces and across membranes (the alveoli).
- Pendelluft: The movement of gas between lung units with different time constants.
- Bulk flow: This may contribute partially to gas exchange as the leading edge of the gas front may actually reach a number of proximal alveoli.

Indications for HFOV

HFOV is primarily indicated as "rescue therapy" in cases of refractory hypercarbia with hypoxemic respiratory failure or severe PARDS.
It is considered when there are high or injurious conventional ventilator setting requirements, specifically when FiO_2 > 60% and Peak Inspiratory Pressures (PIP) $> 30 c m H_{2} O$ .
It serves as a "salvage therapy" in refractory hypoxemic respiratory failure where Extracorporeal Membrane Oxygenation (ECMO) is not available.
HFOV is also indicated in the management of airleak syndromes.
It may be considered in patients with known pulmonary hypertension, severe right ventricular dysfunction, or as a bridge to ECMO.
HFOV has been utilized for neonates and infants with respiratory distress following congenital cardiac surgery, where it demonstrated shorter durations of mechanical ventilation and ICU stay compared to CMV.
Current guidelines do not recommend the routine use of HFOV as an initial strategy for ARDS, advocating for its use solely as a rescue mode when conventional ventilation fails.
HFOV should be considered in children with moderate-to-severe PARDS in whom plateau airway pressures exceed $28 c m H_{2} O$ in the absence of clinical evidence of reduced chest wall compliance.

Preparation Before Starting HFOV

Before initiating HFOV, it is imperative to make a thorough assessment of the patient's respiratory and hemodynamic status.
Auscultation for the character of breath sounds must be done while the patient is still on CMV, because auscultation after transitioning to HFOV may not reveal much.
Suctioning should be performed by an in-line suction system prior to transition in order to avoid derecruitment of the lungs.
During the transition from CMV to HFOV, manual ventilation, preferably with an inline manometer, should be done to deliver pressures as close as possible to the last set CMV settings.
While bagging, the PIP should not exceed 8-10 cm $H_{2} O$ above the MAP on CMV, and a PEEP of 6-8 cm $H_{2} O$ should be maintained as tolerated.
A manual ventilation or recruitment manoeuvre of 35 cm $H_{2} O$ for 35-40 seconds allows the physician to assess the ability of the lungs to be functionally recruited by observing the oxygenation response on the pulse oximeter.
Hemodynamic status assessment prior to transitioning to HFOV must include checking for the adequacy of cardiac output, volume status, and stabilizing blood pressure, as the transition may potentiate hemodynamic instability.

Initial Settings and Goals of Ventilation

Most Pediatric Intensive Care Units use SensorMedics ventilators, deploying the 3100A model for patients less than 35 kg and the 3100B model for patients weighing more than 35 kg.
Patients are usually initially started on conventional ventilation according to lung-protective goals (arterial $p H \geq 7.25$ , $S p O_{2} \sim 88 - 92 %$ , and $P a O_{2} \sim 60 m m H g$ ) before deploying HFOV when the Oxygenation Index (OI) is >15 despite high levels of PEEP.
The $F i O_{2}$ is usually set at 100% (1.0) at the beginning of HFOV and is subsequently weaned based on oxygenation, with an attempt to decrease $F i O_{2} < 60 %$ .
The mPaw is typically set at 5-8 cm $H_{2} O$ above the last mPaw on CMV for a high volume strategy.
If starting HFOV immediately without prior CMV, the clinician should use an mPaw $\approx 8 - 10 c m H_{2} O$ in neonates and $15 - 18 c m H_{2} O$ in infants/children.
The mPaw is then increased stepwise, targeting a saturation of 88-92% and a $P a O_{2}$ of 60 mm Hg.
The mPaw is adjusted specifically to obtain a chest radiograph showing an expansion of nine rib spaces.
The bias flow is set between 20-40 lpm.
The inspiratory time is set at 33% (e.g., 22 milliseconds at 15 Hz, or 41 milliseconds at 8 Hz), making the I:E ratio close to 1:2.
Frequency is set at 5-10 Hz depending on the weight of the child.
As frequency decreases, the total cycle time increases, which increases the duration of electromagnetic force acting on the piston, thus increasing the tidal volume.
Therefore, at any given power, a lower frequency will increase tidal volume and increase alveolar ventilation.
A lower frequency will also increase the total inspiratory time and may improve oxygenation.
The Power setting (Amplitude) is started at 60 (or an Amplitude starting at twice the set mPaw, e.g., 20-25 cm $H_{2} O$ ) and adjusted to achieve an adequate "wiggle" of the chest wall down to the lower abdomen/thighs.
Oxygenation during HFOV is controlled by the Mean Airway Pressure and $F i O_{2}$ .
Ventilation (CO2 removal) during HFOV is titrated by the Peak Inspiratory Pressure (Amplitude) and the Frequency.
Arterial blood gas measurements must be obtained 30 minutes after initiation or any setting changes to guide further optimization.
A chest X-ray should be ordered after 2 hours to monitor the extent of chest inflation.

Recruitment Manoeuvres (RM) on HFOV

Optimal lung recruitment on HFOV should be achieved by a stepwise increment and decrease of the mPaw under continuous pulse oximeter and hemodynamic monitoring.
Immediately after shifting to HFOV, an individualized staircase incremental-decremental mPaw titration may be performed to find the optimal initial mPaw on the deflation limb of the pressure-volume curve.
First, the mPaw is increased by 2 cm $H_{2} O$ from the initial setting every 3-5 minutes while simultaneously observing the $S p O_{2}$ (as a proxy for lung volume) and mean arterial blood pressure.
This increment continues until no further hike in $S p O_{2}$ and/or decrease in mean arterial pressure occurs during two consecutive increments, identifying the onset of lung recruitment.
If during the RM the $S p O_{2}$ exceeds 97%, the $F i O_{2}$ is reduced while continuing the RM.
Next, the mPaw is decreased by 2 cm $H_{2} O$ every 3-5 minutes until the $S p O_{2}$ decreases during two consecutive decrements, establishing the derecruitment mPaw ( $m P a w_{d e r e c r u i t m e n t}$ ).
The "optimal" mPaw is then set at 2 cm $H_{2} O$ above the $m P a w_{d e r e c r u i t m e n t}$ .
The RM must be interrupted if the mean arterial pressure falls below the 5th percentile or if desaturations ( $S p O_{2} < 85 %$ ) occur.
Often, reluctance to perform a recruitment manoeuvre due to physician apprehension of an airleak or barotrauma may result in a failed attempt at HFOV.

Management of Arterial Blood Gases

Clinical Status	Action / Adjustment
Inadequate Oxygenation	If oxygenation is inadequate at initial mPaw ( $18 - 20 c m H_{2} O$ ), obtain a Chest X-ray to assess lung volume. If diaphragms are not flattened (<9 rib spaces), increase mPaw by 2-4 cm every 20-30 minutes until adequate oxygenation is achieved.
Hyperinflation	If Chest X-ray shows hyperinflation, immediately decrease the mPaw by 1-2 cm every 2-4 hours until lung volumes return to normal or oxygenation is adequate.
Hypoxemia	Increase mPaw, increase Amplitude ( $T_{h i g h}$ ), and increase $F i O_{2}$ .
Hypercapnia ( $p H < 7.25$ )	Avoid over-sedation. Try to increase Amplitude ( $P_{h i g h}$ ) and increase Frequency ( $T_{h i g h}$ ). If not improving, decrease Frequency to increase tidal volume delivery.
Refractory Hypoxemia/Hypercarbia	If $S p O_{2} < 88 %$ and $P a O_{2} < 55$ mmHg, increase $F i O_{2}$ and mPaw. Allow to stabilize for 48 hours. Re-assess for hyperinflation on CXR.

Supportive Care and Pharmacotherapy

Spontaneous breathing during HFOV has been shown to improve oxygenation and regional ventilation, but the benefits decline at higher inspiratory flows found in older children.
Therefore, the use of sedative-analgesics and neuromuscular blockade, titrated to the tolerance of mechanical ventilation with appropriate drug holidays, is the norm in most PICUs.
High cumulative doses of vasodilating fentanyl and muscle relaxant infusions are often used to curtail the work of imposed breathing.
This profound sedation can lead to hypotension and a requirement for vasopressors.
A reduction in cardiac output upon initiation of HFOV may lead to increased inotropic requirements in the immediate 24-hour period.
Inhaled nitric oxide (iNO) may be beneficial in improving oxygenation when used as an adjunctive therapy with HFOV.
It appears reasonable to use iNO in patients with known pulmonary hypertension, severe right ventricular dysfunction, or as a bridge to ECMO.

Monitoring, Troubleshooting, and Complications

Nursing care for a patient on HFOV can be challenging; at least two nursing staff must be involved during position changes and in-line suctioning due to the high risk of derecruitment or pneumothorax.
Proper documentation of the "chest wiggle factor" is paramount to early detection of complications such as an obstructed tube, one-sided airleak, or pneumothorax.
A $P a C O_{2} < 35$ mm Hg strongly correlates with an increased risk of pneumothorax.
To minimize the risk of volutrauma, it is critical to use the least amount of Tidal Volume (Power or Amplitude) possible to achieve ventilation.
Most HFOV machines have predefined audible and visual alarm systems, but these have limitations in warning of difficult conditions such as a tension pneumothorax or tracheal tube obstruction.

Complication	Troubleshooting Strategy
Hyperinflation or Barotrauma	Decrease the mPaw.
Secretions	Increase the frequency of suctioning, check humidification, and evaluate for Ventilator-Associated Pneumonia (VAP) if associated with fever, worsening infiltrates, and oxygenation.
Hypotension	Decrease the mPaw, and rule out other causes such as pneumothorax, excessive sedation/analgesia, new-onset sepsis, or fluid restriction.

Weaning from HFOV

A reduction of mPaw is initiated when the $F i O_{2}$ is < 0.5 with a $P a O_{2} \sim 60$ mm Hg.
Once an mPaw $\leq 18 t o 20 c m H_{2} O$ is achieved on an $F i O_{2}$ of 0.4, the patients are returned to CMV.
CMV is typically restarted in the pressure-control mode with the mPaw set close to the mPaw on HFOV, plateau pressures $< 28 c m H_{2} O$ , and PEEP adjusted to deliver a tidal volume of 5-6 mL/kg of predicted body weight.
It is also possible to successfully extubate a child directly from HFOV.
Timely tapering off of sedation, monitoring withdrawal scores, and minimizing the use of muscle relaxants allows for a smooth transition to spontaneous breathing.

Clinical Evidence and Trials

In the neonatal population, a systematic review and meta-analysis summarizing patient data from 10 randomized controlled trials failed to reveal any mortality benefit or decrease in the incidence of Bronchopulmonary Dysplasia (BPD).
However, compared with conventional ventilation, neonatal HFOV use resulted in a reduction in the need for surgical closure of patent ductus arteriosus and a reduction in the risk of retinopathy of prematurity stage 2 or more.
A Cochrane review of elective HFOV comprising 19 studies concluded that HFOV compared to CMV revealed no mortality benefit at 28 to 30 days of age or at approximately term equivalent age.
In adults, the OSCAR study showed similar all-cause 30-day mortality in the HFOV (41.7%) and CMV (41.1%) groups, but noted a higher use of sedatives and muscle relaxants in the HFOV group.
The adult OSCILLATE study was stopped early because it showed a significantly higher mortality in the HFOV group (47%) compared to the controlled ventilation group (35%), alongside a greater requirement for inotropic and vasopressor support.
In pediatrics, the theoretical advantages of HFOV have been challenged as evidence shows it may not entirely protect from volutrauma and atelectotrauma, and the high mean airway pressures may contribute to barotrauma.
The Prone and Oscillation Pediatric Clinical Trial (PROSpect) is a randomized controlled trial currently enrolling patients with moderate-to-severe PARDS ( $O I > 12$ ) to determine whether prone versus supine positioning and HFOV versus CMV will result in an improvement of ventilator-free days.
Despite the lack of apparent widespread mortality benefit in most trials, HFOV remains a critical rescue mode when conventional ventilation has failed, or as the primary ventilation mode of choice as a lung protective strategy in units that strictly protocolize its application.