High Frequency Ventilation

Anatomy and Physiology

During conventional mechanical ventilation, gas transfer happens by bulk transport of gas molecules from large central airways to smaller peripheral airways. This requires a higher tidal volume than dead space ventilation. During HFV, this is not possible as the tidal ventilation delivered is low. One well-known mechanism for gas transfer in HFV is bulk transfer by convection, which may contribute to gas exchange in proximal airways, though it plays only a minor role in peripheral gas exchange.

Turbulence is another method of gas transfer, especially in larger airways. In this theory, the different velocity profiles of asymmetric particles lead to net convective transport. This mode of gas exchange is seen most often in the bifurcation of airways. Taylor dispersion and molecular diffusion are some of the most critical gas exchange mechanisms during HFOV. The other mechanisms described include pendelluft, cardiogenic mixing, and collateral ventilation.[5]

Indications

Indications for HFV in adults and neonates include:

Adults [6]

• It is mainly used in severe ARDS  to prevent VILI. 
• Large air leak syndromes with the inability to keep lungs open  like bronchopleural fistula, pneumothorax, pulmonary interstitial emphysema
• Failure of conventional mechanical ventilation 
• Refractory hypoxemia  as a rescue therapy

Neonates

• Persistent pulmonary hypertension 
• ARDS
• Pulmonary interstitial emphysema 
• Meconium aspiration 
• Pulmonary hypoplasia 

There is no classic recommendation for HFOV in adults. It is mainly used as rescue therapy in severe ARDS. It is used as 1 of the methods to prevent VILI. It is also used in patients with bronchopleural fistula. It is beneficial when ventilation is difficult and lungs cannot be kept open, like pneumothorax and pulmonary interstitial emphysema. It is also used in ARDS due to inhalational injury, blunt trauma chest, and even in patients with traumatic brain injury with high intracranial pressure.[7]

Contraindications

There are no absolute contraindications for HFOV. However, HFOV can be less effective in certain diseases with high intrathoracic pressure and increased airway resistance, like bronchial asthma. It can lead to air trapping and hyperinflation. It can also lead to complications like barotrauma and air leak syndromes like pneumothorax, pulmonary interstitial emphysema, and pneumomediastinum. It can also be avoided in patients with intracranial hemorrhage and severe sepsis with multiorgan failure.[8]

Equipment

There are various brands of HFV devices.[8][9][10]

Personnel

Skilled personnel are necessary to set up the machine and troubleshoot alarms.

Preparation

The machine must be checked for proper functioning, alarms must be set, and the patient's MAP on a conventional ventilator must be noted.

Technique or Treatment

SETTINGS IN HFOV [6]

The set variables are:

1. Respiratory rate/Frequency
2. Amplitude/Power/Delta P 
3. Mean airway pressure (Paw)
4. Bias flow
5. Inspiratory time
6. FiO₂

Frequency 

The rate at which the machine oscillates is set by setting the frequency. A 1 Hz frequency is equal to 60 oscillations per minute. As the inspiration-to-expiration ratio is fixed, tidal volume/amplitude decreases as the frequency increases. Higher frequencies are useful to decrease barotrauma as the pressure change transmitted to alveoli is less at high frequencies. This also increases the zone of safety for ventilation and leads to homogenous aeration of alveoli. The frequency set is usually between 3 to 6 Hz on initiation; it can be as high as 10 to 15 Hz.

Amplitude/Delta P

This is the primary determinant of tidal volume. It occurs due to the piston movement towards or away from a patient's airway. The voltage across the piston, in turn, determines this. Thus, an increase in polarity increases the amplitude and piston movement and, therefore, tidal volumes above the mean airway pressure. In HFOV, inspiration and expiration are both active processes. The amplitude settings are initiated and subsequently adjusted according to PaCO₂ levels. 

Mean Airway Pressure (Paw)

This can be adjusted directly or indirectly. Mean airway pressure is the main determinant of oxygenation, and an increase in Paw improves oxygenation. The settings are adjusted according to oxygenation requirements. Most often, the value initiated is 5 cm of H₂O above plateau pressure in conventional ventilation. Mean airway pressure is adjusted slowly based on saturation in increments of 2 cm H₂O. However, the maximum value is 35 cm of H₂O, and the usual targets are less than 30 cm of H2O.

Bias Flow

This is the gas flow rate in the ventilator and the circuit apparatus. In HFV, the bias flow is usually around 40 L/min to a maximum of 60 L/min. An increase in bias flow is an indirect method of increasing MAP and oxygenation. The bias flow needed is high in patients with air leak syndromes.

Inspiratory Time

The inspiratory time set is always less than 50% of the total respiratory cycle, and most often, it is set at 33%. An increase in inspiratory time increases mean airway pressure and thus improves oxygenation. However, it can increase the risks of barotrauma; thus, it is mostly kept constant.

Initial Setting for HFOV [8]

The initial settings are a primary guide and must be adjusted according to subsequent arterial blood gas and clinical assessment. The initial parameters are usually set as below:

1. Bias flow is usually set from lower values, starting from 20 L/min to 35 L/min, and is adjusted subsequently as per the patient’s needs.
2. Inspiratory time is often constant and is set at 33%, giving an inspiration-to-expiration ratio of 1 to 2.
3. Respiratory rate/frequency are the main determinants of PaCO₂ and are set between 3 to 15 Hz. It is most often initiated at 5 to 6 Hz, giving a respiratory rate of about 300 per minute. Subsequent adjustments are made by serial ABG monitoring.
4. The amplitude (ΔP) is the primary determinant of tidal volume and is initiated and titrated by looking for chest wiggles/vibrations. In infants, a chest wiggle up to the umbilicus is targeted, whereas in children and adults, chest wiggles up to the pelvic region and the mid-thigh are targeted, respectively. It is usually set at about 20 to 30 cm H₂O higher than patients' PaCO₂ on conventional ventilation.
5. FiO₂ and mean airway pressure settings mainly determine oxygenation. When initiating HFOV, the mPaw is set at 5 cm H2O above the mPaw seen on a conventional ventilator. FiO₂ is initially set at 1.0 and subsequently tapered as per the patient's oxygenation requirements, titrated to a target SpO₂ of 88 to 92%. Some patients may need a recruitment maneuver before initiating HFOV.

Weaning from HFOV [8] 

Weaning from HFOV is not based on fixed protocols, and various methods are followed. The process involves weaning to an extent where the patient can tolerate conventional ventilation. The parameters that determine weaning readiness are FiO₂ and mean airway pressures. Once oxygenation goals are met, 2 steps can be followed. The first step is to wean FiO₂ to less than 60%, considering a saturation of more than 88%, and the next step is to decrease MAP in increments of 2 cm H₂O to achieve a MAP of 30 cm H₂O. 

1. Once the above is done, the next step is to slowly wean FiO₂ to 0.4 and the MAP in increments of 2 cm to reach a final goal of 20 to 25 cm H₂O.
2. After achieving the above, the next approach is to transition the patient to conventional lung-protective ventilation and target saturation of more than 88% with mPaw of 20 to 25 cms for the next 24 hours. 
3. Weaning failure is considered when the patient is weaned to conventional low tidal volume ventilation and fails to maintain saturation above 88% in the initial 48 hours.

Complications

 HFV is not without complications. The following are the challenges faced in HFV:

• Its efficacy is questionable in patients with high airway resistance and can lead to air trapping and barotrauma like pneumothorax, pneumomediastinum, pneumopericardium, and pulmonary interstitial emphysema.[11]
• It can also cause harmful heart-lung interactions and lead to high intrathoracic pressures, thus causing decreased venous return and cardiac output.[12]
• As it is an unorthodox ventilation method, it leads to decreased clearance of secretions and higher risks of secondary sepsis.[11]
• Other limitations include transport difficulties, noisy machines causing problems in clinical examinations, and delayed identification of complications.[12]

Clinical Significance

Mechanical ventilation, despite the unavoidable need, tends to cause ventilator-induced lung injury. In positive pressure ventilation, the most common mechanisms that lead to lung injury are barotrauma, volutrauma, and atelectrauma (due to repeated opening and closing of alveoli). Thus, high tidal volumes and high pressures (plateau and peak air pressures) cause and aggravate ventilator-induced lung injury. The most proven preventive method is low tidal volume ventilation, as proposed by the ARDS network.[13] In HFV, this is avoided as the entire aeration cycle operates in the safe zone, thus preventing overdistention, which causes VILI. It also prevents derecruitment and avoids atelectrauma and barotrauma. It prevents barotrauma and helps improve the ventilation-to-perfusion ratio by allowing uniform aeration of the lungs.[6] The tidal volume used in HFOV is less than dead space volume, preventing cyclical opening and closing of alveoli. By this, it delivers a constant MAP, thereby reducing VILI. It also helps in recruitment by using high positive end-expiratory pressure.

Few trials have been done to study the risks and clinical benefits of HFOV  in ARDS. In the OSCILLATE trial, adult patients with moderate to severe ARDS were randomized to receive conventional ventilation with ARDS  protocol or HFOV. This study noted significantly higher mortality in the HFOV group (41%) than in conventional ventilation (35%). The trial concluded that early institution of HFOV  in moderate to severe ARDS was not beneficial and could be harmful.[14] The OSCAR randomized control trial was a multicenter study in the UK in patients with severe ARDS. It proved that there was no difference in mortality between the study groups, and HFO may not be beneficial.[15] The RESTORE study done in pediatric ARDS patients found that the use of HFOV in ARDS  led to increased sedation requirements and length of ICU stay.[16] A meta-analysis published in 2017 analyzed that HFOV was not useful but could be potentially harmful when used in mild to moderate ARDS with higher PO₂/FiO₂ ratios. However, its use as a potential modality, mainly as rescue therapy in refractory hypoxemia, is still considered beneficial. Thus, in patients with severe ARDS with refractory hypoxemia, the use of HFOV may help, especially when proning and ECMO are impossible or unavailable.[17]

Enhancing Healthcare Team Outcomes

Successful execution of HFV highlights the role of the interprofessional team in evaluating and improving care for patients who need close coordination and cooperation between various healthcare providers & specialty teams. HFV is currently accepted only as a rescue strategy in refractory hypoxemia, where other conventional or supportive options are impossible or unavailable. The decision to utilize HFV must be made after close interaction and coordination between the intensive care, pulmonology, and respiratory therapy teams. Biomedical or technical assistance may be required at the bedside due to a lack of experience and familiarity with this ventilatory mode among many providers. Close interaction and coordination between various healthcare professionals indisputably bring out the best outcome for the patient.