2012 OPEN FORUM Abstracts
THE EFFECT OF APRV VENTILATION ON INTRACEREBRAL PRESSURE AND CEREBRAL HEMODYNAMICS : A CASE REPORT.
Stephen Sibole1, Paul Marik2,1; 1Respiratory Care, Sentara Norfolk General Hospital, Hampton, VA; 2Department of Intensive Care Medicine, Eastern Virginia Medical School, Norfolk, VA
Introduction: Airway pressure release ventilation (APRV) is a ventilation strategy incorporating the open lung concept, which is often associated with a higher mean airway pressure (MAP) than conventional low tidal volume ventilation. Classic teaching suggests that elevated MAP impedes venous return which may increase intracerebral pressure (ICP). Several studies have determined an association between PEEP and ICP and have concluded that influences to ICP and cerebral blood flow are a function of lung compliance and distention. In this case, we present a patient who suffered a sub-arachnoid hemorrhage (SAH) with a ventriculostomy in place, who was transitioned from pressure-controlled mandatory ventilation (P-CMV) to APRV due to progressive hypoxemia. Case Summary: A 68 year-old female with hypertension, and coronary artery disease, presented with sudden onset of headache, nausea and vomiting, and a syncopal episode. A non-contrast CT and CT-angiography of the head and neck revealed a ruptured large basilar arterial terminus, multiple intact small intracranial aneurysms, and significant intraventricular hemorrhage with enlarged ventricles. The patient underwent a ventriculostomy and coil embolization within eight hours of presentation and was admitted to the neurological ICU for post-intervention management. Post-operatively the patient was initially asymptomatic; however, within 72 hours developed altered mental status and respiratory distress requiring intubation and mechanical venitlation. She required increased ventilator support with the following ventilator settings: P-CMV with PC of 20 cm H2O, PEEP of 8 cm H2O (MAP of 10 cm H2O), set respiratory rate of 12 bpm and FIO2of 1.0. Due to refractory hypoxemia and atelectasis, the mode of ventilation was changed to APRV with the following settings: PHigh 26 cm H2O, FIO2 titrated to 70% based on the SPO2, THigh 5 sec, TLow 0.8 sec (termination of expiratory flow of 50%), with a MAP of 22 cmH2O. Extensive cerobro-hemodynamics monitoring was obtained before and after the change in mode of ventilation. Discussion: In this case, we demonstrate that the use of APRV, in a patient with close to normal static lung compliance (50mls/cm H2O), was effective in improving oxygenation without significantly elevating ICP. This patient ultimately survived and was liberated from mechanical ventilation. Sponsored Research - None