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The conventional ventilator is initially set up using PCV with an I:E ratio of 1:1 and 12 cmH2O PEEP with a respiratory rate of 20 - 25. The mean airway pressure, inspiratory plateau pressure, and delivered tidal volume are immediately checked when the patient is changed to the conventional ventilator and small adjustments to PEEP or pressure are made to ensure that the mPaw is within 2 -3 cmH2O of what it was on HFOV. When the mean airway pressure is closely matched to what it was on HFOV we have found that most patients are easily transferred to conventional ventilation and are able to maintain a SpO2 > 90% on the same FiO2. An arterial blood gas is obtained 15 - 20 minutes after transfer to conventional ventilation to guide further ventilator adjustments. 7. Other Supportive Issues During HFOV Sedation and Paralysis During HFOV, the patient is kept deeply sedated with a combination benzodiazepine (e.g. lorazepam, midazolam), and narcotic (e.g. fentanyl, morphine) infusion. Prior to initiation of HFOV, the patient is also pharmacologically paralyzed with a long acting neuromuscular blocker (e.g. cis-atracurium). Many patients are already paralyzed on conventional ventilation prior to being placed on a trial of HFOV and if so, the paralysis is continued. A nursing protocol for care of the paralyzed patient is essential to ensure comprehensive care of the patient (e.g. skin care, ankle splints, mouth care, etc). It is important to recognize that sinus tachycardia or hypertension developing during HFOV may indicate inadequate pain relief or sedation in a paralyzed patient. As patients are weaned from HFOV and are approaching transfer back to conventional ventilation we have observed that continued neuromuscular paralysis may not be necessary. As the mPaw is approaching 20 – 24 cmH2O, we have tried discontinuing the paralytic agent while continuing sedation and analgesia with success. Once stabilized on HFOV, some patients may be managed with sedation and analgesia alone. Typically, patients have not required continued paralysis after transfer back to pressure control ventilation with an I:E ratio of 1:1. We have also substituted propofol for the benzodiazepine as an adjunct to sedation as weaning is progressing. Propofol may allow quicker “wake-up” times to permit trials of spontaneous breathing on pressure support ventilation during the final phase of weaning from conventional ventilation. Nevertheless, one may anticipate prolonged sedation and muscle weakness after many days or weeks of benzodiazepine and neuromuscular blocker drug infusions that may limit final extubation even when oxygenation is no longer an issue. Suctioning and Bronchoscopy Tracheal suction should be done prior to initiation of HFOV. During the early hours and days of HFOV we try to limit interruption of HFOV to perform suctioning unless there are gross secretions in the airway or evidence of atelectasis on chest radiograph. Tracheal suction lowers L1856 Rev. A November 2001 10 carinal pressures and may allow alveolar derecruitment to occur - usually manifested as a lower SpO2 or requirement for a higher FiO2. Additionally, placement of an inline right-angle suction adapter in the HFOV circuit may impair the delivered waveform and impair ventilation. For this reason, we recommend attaching the HFOV circuit directly to the endotracheal tube (without an inline suction adapter) until it is clear that adequate PaCO2 elimination can occur. If required, bronchoscopy can be performed during HFOV through a right angle adapter or during a brief interruption of HFOV. In unstable patients requiring high FiO2, the duration of the bronchoscopy should be as brief as possible. Deep vein thrombosis prophylaxis Patients on HFOV are deeply sedated and pharmacologically paralyzed during the initial phases of their illness. The lack of mobility puts these patients at increased risk for thromboembolism. For this reason, we aggressively use pneumatic boots, compression stockings, and subcutaneous low dose heparin if no contraindications exist (e.g. intracranial hemorrhage, recent spinal surgery). We favor the use of prophylactic dose low molecular weight heparin (e.g. enoxaparin 30 mg SQ bid or 40 mg SQ q day) since it has a reportedly lower incidence of heparin-induced thrombocytopenia. In addition to aggressive attempts at prophylaxis for deep vein thrombosis we also use lower extremity ultrasound screening every 72 to 96 hours to look for clot development that would require full anticoagulation or caval filter placement. Summary HFOV is an important alternative method of mechanical ventilation for severe ARDS in large patients. It should be considered for use in patients requiring high mPaw (≥ 24 cmH2O) on conventional ventilation – especially if the FiO2 requirements exceed 60% and Pplat is unable to be maintained ≤ 30 – 35 cmH2O. Failure to improve the oxygenation index within the first 24 – 48 hours is indicative of a poor response to HFOV. In our experience, nonresponders to HFOV have an extremely high mortality from ARDS – approaching 100%. Late phase fibroproliferative ARDS, when the alveolar architecture is severely damaged, is less likely to respond. Adjunctive therapies that are currently being investigated in combination with HFOV include prone positioning, nitric oxide, aerosolized prostacyclin, surfactants, and partial liquid ventilation. All of these adjunctive therapies have been demonstrated to improve oxygenation, however, whether mortality or ventilator-free days in adults will be improved awaits demonstration by randomized, controlled trials.