The combination of high-frequency ventilation and recruitment maneuvers results in rapid and sustained improvement in oxygenation.
The management of ARDS has changed over the last several years. Many treatment techniques have been tried, but the greatest improvement has been in how we ventilate patients and the prevention of further ventilation induced lung injury (VILI). Acute lung injury (ALI) and adult respiratory distress syndrome (ARDS) are characterized by severe inflammation and coagulation that induces permeability changes in the alveolar capillary membrane. Protein-containing fluid shifts into alveolar and interstitial spaces causing the horrible pathology of these diseases.1 This process of fluid shifting into the interstitium and alveoli results in a form of noncardiogenic pulmonary edema.2 Both ARDS and ALI are acute in onset and are seen with relatively normal pulmonary capillary wedge pressures and bilateral infiltrates on chest radiographs. ALI is defined as a Pao2/Fio2 ratio of 300 mm Hg, while ARDS has a more severe ratio of 200 mm Hg. If promptly recognized, ALI is reversible in the early stages.2 Standard treatment strategies include lower tidal volumes using mechanical ventilation and ICU support to prevent further multi-organ dysfunction once the inflammation has been triggered.
The clinical trial by the National Institutes of Health and ARDS network (ARDSnet) reported a low tidal volume strategy as a lung protective approach (lung tidal volume of 4-6 mL/kg of predicted body weight and an inspiratory plateau pressure of 30 cm H2O) on conventional ventilation (CV).3 This reduced the absolute mortality by 9% when it was compared with larger tidal volume ventilation. To correct this, we realize we may have to utilize a higher rate, a higher Fio2, and probably a higher positive end-expiratory pressure (PEEP). These compromises may themselves be a detriment, but as of yet this has not been totally proven. Regardless, with this volume ventilation we still get cyclical opening and closing of compromised alveoli. Unfortunately, in practice, many critically ill patients with ARDS are unable to achieve adequate gas exchange using conventional lung protective strategies, and the mortality is still extremely high.4
There is not a perfect mode of mechanical ventilation for ALI/ARDS; however, having a mode of ventilation that allows continuous noncyclical positive pressure with tiny tidal volumes along with active inspiration and expiration may be the ideal type of ventilation. High frequency oscillatory ventilation (HFOV) may fit these criteria. The potential benefits of HFOV over CV are seen in animal studies. HFOV improved gas exchange as well as lung inflation and decreased VILI in surfactant-deficient rabbits and primates.5-8 In review of these trials, the reduced cyclical alveolar collapse and overdistension are prevented by the use of HFOV. This mode of ventilation was associated with reduced levels of inflammatory mediators compared with CV techniques even with similarly high levels of mean airway pressure.9-11
In the pediatric population, HFOV has been shown to improve oxygenation and reduce VILI compared with CV.12,13 This use of HFOV led to improved mortality with a lower incidence of VILI and reduced O2 requirements in a study of low birth weight infants.14 This trial demonstrated a reduced mortality and fewer mechanical ventilation days in those infants assigned to HFOV.
In adult patients with ARDS, HFOV has been studied and reported in several observational trials and a few randomized controlled trials. The studies showed a significant improvement in oxygenation using an open lung strategy. Outcomes were shown to be better if HFOV was used early in the ARDS disease process.15-18 Derdak et al19 completed a multi-center, randomized controlled trial (MOAT) comparing HFOV with conventional pressure control ventilation in 148 patients. The trial demonstrated a trend toward reduced mortality in the HFOV arm and a marked improvement in the Pao2/Fio2 ratio. The authors concluded that HFOV is a safe and effective mode of ventilation for the treatment of ARDS in adults.19
HFOV Gas Transport/Exchange Mechanisms
Gas transport and exchange in HFOV differ greatly from their counterparts in conventional ventilation. The transport/exchange mechanisms in conventional ventilation include dead-space volume (where convective transport is the primary method) and alveolar ventilation (where molecular diffusion is the primary mechanism).20 HFOV uses multiple gas flow/exchange dynamics, including bulk convection, asymmetric velocity profiles, pendelluft, cardiogenic mixing, Taylor dispersion and turbulence, molecular diffusion, and collateral ventilation. All of these mechanisms have a contributory role in gas exchange in HFOV, and they probably work in combination to enhance gas transport and exchange in HFOV.21-23
With the beneficial reports of HFOV in neonates and pediatric patients, we began using HFOV as true salvage therapy for late stage ARDS in critically ill trauma and surgical patients. Though used late in the course of the disease, this mode of ventilation seemed to improve mortality in some patients.
The exact threshold for initiation of HFOV remains unclear. At Carolinas Medical Center, we generally consider using HFOV in the trauma/surgical population for patients requiring a Fio2 of 60% or more, PEEP levels of 12 to 16 cm H2O, and a mean airway pressure (mPaw) range of 20 to 24 cm H2O for whom an inspiratory plateau pressure of 30 to 35 cm H2O cannot be maintained. We use HFOV in the operating room as the initial mode of mechanical ventilation after injury if severe trauma or factors highly indicative of ALI or ARDS, such as pulmonary contusions or massive crystalloid/blood resuscitation, are present.
Before HFOV is initiated, several factors must be taken into consideration. It is important for the airway to be patent and appropriately cleared via suction. Secretions, narrowing, or obstruction of the airway, trachea, and mainstem bronchi must be addressed before HFOV begins, as these factors will disrupt delivery of the oscillatory waveform and impede ventilation.
Adequate sedation and analgesic medication should be given prior to initiation of HFOV. Intermittent doses of a neuromuscular blockade drug may be used during initiation, and if agitation or desaturation occurs. An attempt should be made to minimize the use of neuromuscular blockade drugs.24,25
Intravascular volume should be constantly assessed prior to and during HFOV. Use of a higher sustained mPaw with HFOV can cause hypotension secondary to the elevated intrathoracic pressure and reduced preload. Hemodynamic monitoring, echocardiography, and use of a pulmonary artery catheter may help optimize hemodynamics and cardiac function.26
Our experience was presented at the Western Trauma Association in March 2005. We have seen that hemodynamic monitoring is beneficial in these patients with ALI and ARDS, but pulmonary artery wedge pressure is falsely elevated with the increase in mPaw associated with HFOV. Using end diastolic volume indices (EDVI) as an indicator of vascular volume, we showed no false alterations in values when associated with a higher mPaw. When maintaining adequate EDVI values, trauma and surgical patients with ALI/ARDS did not have negative hemodynamic events associated with the rise in mPaw.
In addition, the survivors of ALI/ARDS at our institution when HFOV is used had fewer days on conventional ventilation (3 days for survivors versus 7 days for nonsurvivors). This is consistent with other reported outcomes.4,18-19
Our initial settings follow manufacturer guidelines,26 using an mPaw 4 to 5 cm H2O higher than conventional ventilation settings to achieve an open lung.4,27 If hemodynamic instability is seen, the initial mPaw will be reduced to a level 2 to 3 cm H2O higher than or equal to the mPaw for conventional ventilation. For patients who are stable hemodynamically, an initial recruitment maneuver is performed by increasing the mPaw to 40 to 45 cm H2O for 40 seconds with the piston turned off.28 If severe oxygenation problems exist, the inspiratory time percentage control will be increased to 50% from an initial 33% to raise the distal alveolar pressure slightly nearer the set mPaw. Oxygen is initiated at an Fio2 of 100% and decreased to maintain an oxygen saturation of 88% or more. If refractory oxygenation exists, hemodynamic status is reexamined and recruitment maneuvers are repeated.28 Lung recruitment and improvements in oxygenation may take several hours to achieve; patience and vigilance are suggested during the initiation phase.
Ventilation and Weaning
Ventilation is controlled by frequency (Hz) and power (amplitude). Support is usually initiated at 5 Hz, and power is adjusted to achieve a amplitude 20 to 30 cm H2O higher than the most recent arterial blood gas Paco2. Attempts are made to achieve an arterial pH of 7.2 or more. In the trauma/surgical population at our institute, once we have reached 4 Hz and power has reached 8, we employ a tracheal tube cuff leak to aid ventilation.4,29 Neonatal applications of HFOV commonly use an uncuffed endotracheal tube. A cuff leak has been used in high-frequency percussive ventilation/volumetric diffusive respiration to achieve better ventilation and secretion clearance.30,31 This technique involves removing air from the cuff until the mPaw decreases 5 to 8 cm H2O, then returning the mPaw to the desired setting. We use a cuff leak early to minimize possible overdistension that is thought to be seen at low frequencies with high amplitudes. Bias flow may need to be increased to achieve the desired mPaw.4
Weaning starts very shortly after HFOV initiation, in the form of decreasing the Fio2. Once chest-film improvement is seen, we decrease the mPaw in increments of 1 to 2 cm H2O over 12 hours. It has been our experience that decreasing the mPaw quickly can result in lung derecruitment, with the end result of increasing the mPaw and thus prolonging weaning. For ventilation, our goal is to ventilate with the highest frequency and the lowest power setting achievable. It has been our experience that ventilation is usually a problem when lung derecruitment occurs, or when hemodynamic compromise is present. In most cases, when the mPaw has reached 18 to 20 cm H2O, we convert to conventional ventilation. Our default mode is pressure control or pressure-regulated volume control, with PEEP set at 12 to 14 cm H2O, respiratory rate set at 14 to 24 breaths per minute, and a tidal-volume goal of 6 to 8 mL/kg with inspiratory plateau pressures of 30 to 32 cm H2O. We have also used airway pressure release ventilation as a transitional mode, initiating it with high and low pressures of 24 and 0 and high and low times of 4 to 4.5 seconds and 0.7 to 1 second.32,33
Complications and Considerations
During HFOV, pneumothorax and tension pneumothorax may cause no changes in displayed mPaw or amplitude. Breath sounds are difficult to assess due to transmitted piston sounds and the delivery of very small volumes. Hypotension and hypoxemia may be the first indications of pneumothorax, so a high index of suspicion is imperative. If time permits, chest radiography should be performed immediately; if there is doubt, and patient instability exists, insertion of a chest tube on the side where the pneumothorax is suspected is suggested.
Occlusion of the tracheal tube is of paramount concern in HFOV. A small occlusion can cause an abrupt rise in Paco2. Vigilance and adequate humidification and suction are required to maintain a patent airway. We use a closed suction catheter system with HFOV, with great success. If suction by normal means will not clear secretions, bronchoscopy should be considered. If cuff leaks are routinely used, attention should be paid to the upper airway. Secretions, as well as edema above the tracheal tube, can cause hypercapnia, even with a cuff leak.
Nominal changes in proximal amplitude or mPaw are seen accompanying changes in lung compliance. Increases in displayed amplitude with no changes in mPaw may indicate a sudden decrease in lung volume or an increase in airway resistance.34 A decrease in mPaw with no change in amplitude may indicate a new or intensifying air leak. A decreasing amplitude at a constant power setting may be an indication of expanding lung volume.
If hemodynamic instability is not a concern, elevating the head of the bed to approximately 30° is acceptable. Continuous lateral rotation can be performed successfully, as the patient tolerates it. As a rule, we will not elevate the head of the bed or perform lateral rotation until 24 hours after initiation of HFOV to allow for optimal lung recruitment. The use of nitric oxide in conjunction with HFOV may allow acute improvements in oxygenation to provide a critical temporary bridge to possible recovery. Prone positioning in conjunction with HFOV (with and without nitric oxide) has been shown to improve oxygenation in critically ill patients, but it has not been shown to improve mortality.35-37 Research is needed to determine the effects of prone positioning and nitric oxide on mortality and on lengths of stay in the intensive care unit.
Oxygenation has multiple reports of improvement with application of inhaled nitric oxide. The use of nitric oxide in conjunction with HFOV may allow acute improvements in oxygenation to provide a critical temporary bridge to possible recovery. However, there are currently no reports of decreased mortality utilizing nitric oxide in conjunction with HFOV.35, 36 Nitric oxide should receive increased research to determine its effects on ICU length of stay, as well as mortality, in ALI/ARDS.
The use of aerosolized medications in conjunction with HFOV has very little reported effectiveness. Metered-dose inhalers seem to be ineffective in producing optimal drug deposition.38 Use of flow-driven nebulizers attached to the HFOV circuit has not been studied thoroughly. It is known that the use of flow-driven nebulizers will result in alterations in mPaw and amplitude, which will require adjustment of these variables by clinicians to maintain stable HFOV settings.39 Promising results with HFOV have been reported40 for an aerosol generator that uses a vibrational element to produce an aerosol. Much attention is focusing on the delivery of agents (in addition to aerosolized bronchodilators) that may promote pulmonary vasodilation, aid in pulmonary edema clearance, and transform lung reparative processes.23
Transport and Intervention
Repeated trips to the operating room are required for procedures that cannot be performed in the ICU. At our facility, we have initiated HFOV for multiple trauma patients in the operating room as a rescue method. Based on our experience, we feel that removing these patients from HFOV for transport would be detrimental, especially since lung recruitment, improving hemodynamics, and improved oxygenation/ventilation result from our early intervention. With proper thought and planning, transport on HFOV within the hospital can be safely performed. We have successfully transported many patients on HFOV from the operating room to the ICU and from the ICU to the operating room.42
HFOV has been perceived as a barrier to operative intervention in critically ill patients due to the chest motion involved and to their critical illness or instability. We have successfully and safely performed operative procedures on patients receiving HFOV, however. Procedures such as abdominal exploration, vascular surgery, tracheostomy, bronchoscopy, central-line placement, insertion of inferior vena cava filters, transesophageal echocardiography, and tissue debridement have been performed by our surgical/critical care team.43
William S. Miles, MD is director of surgical critical care, medical director trauma/ICU; and Joseph Hylton, RRT-NPS, CPFT, NCEMT, RCP, is manager, trauma/surgical division, respiratory care services, Carolinas Medical Center, Charlotte, NC.
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