You’re probably aware that acute lung injury and acute respiratory distress syndrome (ALI/ARDS) carry a high mortality. But you may not know that high-frequency oscillatory ventilation (HFOV) can be used as a lung-protective strategy and rescue mode for patients who have this syndrome of acute, persistent lung inflammation with increased vascular permeability.
To maintain effective oxygenation and ventilation, patients with ALI/ARDS require measures to protect the lungs, such as HFOV. Used for neonatal, pediatric, and adult forms of respiratory failure, HFOV differs from conventional mechanical ventilation by maintaining open lung volume through a constant mean airway pressure to achieve effective oxygenation, while oscillation removes CO2. HFOV has been studied across all patient ranges as a lung-protective strategy for ALI/ARDS refractory to conventional ventilation.
How HFOV works
HFOV delivers a constant flow of heated, humidified gas, providing flow rates of 20 to 60 L/minute. This flow produces a constant applied airway pressure or mean airway pressure (mPaw) similar to that of high-flow continuous positive-airway pressure (CPAP).
Typically, mPaw is set at 25 to 35 cm H2O to maintain adequate lung volume for effective oxygenation. It may be adjusted by changing either the flow rates delivered to the system or the pressure threshold of the mushroom valve, which controls outflow of gas from the system.
An oscillating piston pump similar to the woofer of a loudspeaker vibrates the pressurized gas at a frequency that’s generally set between 3 and 15 Hz (1 Hz = 60 cycles/minute). As the “speaker” moves forward and backward, a portion of the flow is displaced in and out of the circuit and the patient respectively.
The power setting (amplitude) on the ventilator controls the distance the “speaker” travels from its resting position, which controls displaced tidal volume (VT). This oscillatory pressure amplitude, or delta P (∆P), is titrated to achieve acceptable CO2 elimination.
Indications and contraindications
HFOV may be indicated when ALI/ARDS doesn’t respond to conventional mechanical ventilation therapies, such as intermittent recruitment maneuvers with positive end-expiratory pressure or pressure-control ventilation. Controlling mPaw to maintain adequate lung volume may mitigate the risk of repetitive airspace opening and closing.
Potential contraindications for HFOV include obstructive lung disease and intolerance to the heavy sedation or neuromuscular blocking agents (NMBAs) that this method generally warrants. HFOV also may be contraindicated in patients with traumatic brain injuries and increased intracranial pressure, as CO2 removal may be difficult to achieve.
During the patient’s initial transition to HFOV, mPaw typically is set 5 cm H2O above the mPaw of the current setting on conventional ventilation. Because HFOV is more suitable for maintaining than recruiting lung volume, an initial recruitment maneuver should be performed as an adjunct before the transition from conventional ventilation.
Initial ∆P is titrated upward until a visible “wiggle” of the patient’s body from shoulder to mid-thigh occurs. The frequency commonly is initiated at 5 Hz in adults, with inspiratory time set to 33%.
To improve oxygenation, mPaw and inspiratory time may be increased. However, increasing the inspiratory time may cause CO2 to rise as well. CO2 clearance can be enhanced by increasing ∆P or decreasing Hz, as both maneuvers tend to increase cycle VT. Also, creating an intentional cuff leak by removing air from the artificial airway balloon may improve CO2 clearance by washing out the dead space with the bias flow. Because a cuff leak can lower mPaw and decrease oxygenation, the bias flow is titrated upward until pre–cuff-leak mPaw is achieved.
The nurse’s role during HFOV
If your patient is receiving HFOV, you’ll need to carefully auscultate heart and breath sounds, perform suctioning, provide humidification, and monitor for CO2 retention and adverse effects of sedatives or NMBAs.
Before auscultating heart and breath sounds, a respiratory therapist or other qualified practitioner may need to stop the piston to reduce artifact. This is best done in a controlled situation, with one clinician controlling the ventilator as the other auscultates. Be aware that when the Hz level is turned to zero to stop the piston, the patient is functionally on CPAP. Although CPAP maintains mPaw and recruitment and minimally affects oxygenation, CO2 levels will rise unless the piston is restarted promptly.
Before an open-suction catheter system is used, the clinician must disconnect the patient from HFOV. Keep in mind that mPaw disruption causes derecruitment, requiring an increased fraction of inspired oxygen and possibly recruitment maneuvers to regain lost lung volume.
Use of a closed-system suction catheter, which doesn’t necessitate disconnection, may reduce the derecruitment risk. However, heavy sedation or NMBAs suppress the natural cough reflex. A suction catheter doesn’t reach very far, so distal airways are absent from pulmonary hygiene, possibly necessitating serial bronchoscopies for secretion removal.
Because of the high gas-flow rate, humidification is critical during HFOV. Make sure active humidification is functional and fluid bags for the humidification system are never empty.
The high flow also can desiccate secretions and cause necrotizing tracheobronchitis, resulting in occlusion and damage to both the artificial and native airways. Typically, this condition manifests as a sudden CO2 increase and a visible change in the magnitude of the thoracic wiggle. If acute CO2 elevation occurs, the cause must be investigated (as with bronchoscopy) to rule out complete or partial airway obstruction.
CO2 retention is another potential complication of HFOV. If you use an intentional cuff leak to enhance CO2 removal, keep the patient’s mouth and posterior pharynx clear of secretions to prevent them from spraying. Always wear protective gear, such as a mask and eye shield, while at the patient’s bedside.Monitoring for adverse drug effects
Closely monitor for adverse effects of sedatives, NMBAs, or both as appropriate. Some patients may need volume resuscitation and vasoactive agents to counter the adverse effects of heavy sedation and mPaw. As needed, use a sedation/agitation scale to monitor sedation effects. A train-of-four protocol should be in place to monitor NMBA effects.
Starting HFOV early in patients with acute respiratory failure can blunt the continued derecruitment seen in this condition. To improve your patient’s chance of survival, always perform vigilant nursing observation and care during HFOV. O
Bernard G, Artigas A, Brigham K, et al. The American-European Consensus Conference on ARDS: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med. 1994;149:818-824.
Penny L. Andrews, BSN, RN, is a Full Partner in the Neurotrauma Critical Care Unit at the R Adams Cowley Shock Trauma Center at the University of Maryland Medical Center in Baltimore. Nader M. Habashi, MD, is Medical Director of the Multitrauma Critical Care Unit at R Adams Cowley Shock Trauma Center.