2002 OPEN FORUM Abstracts
HIGH FREQUENCY VENTILATION IN A CASE OF HEMODYNAMIC INSTABILITY AND PULMONARY EDEMA
Dawn Burks RRT,
Jason Higgins RRT, Grant OKeefe
Surgical/Trauma ICU, Parkland Hospital, Dallas, Texas
Introduction: High Frequency Ventilation use in a patient with pulmonary edema and hypoxia that lead to repeated codes requiring ACLS intervention 6 times in approximately 12 hours.
Case Summary: A 62 yr old Hispanic male was admitted to the Parkland ER, with leg and pelvis fractures on a 100% non-rebreather mask. His medical history was diabetes x3yrs. He was hypotensive and given multiple fluid boluses and blood products. Seven hours later he appeared in obvious respiratory distress, sats dropped, and BLBS revealed crackles throughout. An ABG indicated PaO2 of 53mm Hg. The patient was intubated and a Swan-Ganz catheter was placed. The patient?s initial Cardiac output (CO) was 2.61L/min and SVO2 60mm Hg. Hypotension continued to be managed with fluids and blood products. Four hours later the patient?s HR dropped to 34 bpm, BP 40/30, 0 pulse. ACLS protocols began with positive results and vasopressors were started. Sixteen hours post arrival, despite aggressive ventilator management, serial ABGs revealed no significant improvement in PaO2 and Swan readings show a slight increase in CO (3.4L/min) and an SVO2 of 57%. Patients fluid balance was positive 18L, urine output was minimal, and the patient continued to require ACLS intervention for the next six hours. Over the next fourteen hours, the patient experienced fulminating pulmonary edema despite PEEP levels exceeding 25 cm H2O. ETT suctioning at this time only decreased mean intra-thoracic pressures and allowed for worsening pulmonary edema. The decision was made to place the patient on HFOV 3100A with these initial settings: MAP 37, Power 10 with a resultant Amplitude of 60, HZ 5, I-time % of .50 , and an FiO2 100%. The patient?s oxygen index at this point was 76 which was 30 greater than the 100% fatality group observed in the Fort HFOV study. Additionally, no significant improvement in ABGs or Swan readings were noted and ACLS intervention was still required. Over the next three hours, while the initial CXR attempt was not tolerated, vital signs began to improve. There was no more evidence of pulmonary edema in the ETT. Cardiac output increased to (4.8L/min), SV increased from 19ml/beat to 28ml/beat, and SVO2 climbed to 71%. The patients urine output was increasing and vasopressors were weaned. After eight hours on HFOV a second CXR was successful and revealed the patient?s diaphragm at T10 in the right lung mid-clavicular representing overdistension. Consequently, MAP was decreased to 35cm H20. One hour later the ABG showed 7.48/31/157/23/-0.2/02 sat 97%. At this time MAP was decreased to 30cm H20 and the FiO2 decreased to 60% with a follow up ABG showing a PaO2 of 121. Ventilator weaning continued as blood gasses and diaphragm placement indicated. Over the next 24 hours all cardiovascular drips were discontinued. Vent settings weaned as clinically indicated by blood gasses and diaphragm location shown on CXR. The patient returned to conventional ventilation approximately 72 hours after initiation of HFOV, and was transferred to the floor several weeks later.
Discussion: This case may point to another indication or benefit of using HFOV where high MAPs are required. The patients pulmonary edema was so severe that it was impossible to oxygenate him conventionally. His injuries and tenuous hemodynamics did not allow for prone positioning. The immediate effect of higher MAP may have been a large factor in treating his hypoxemia and thus ending his need of ACLS. It seemed that some hemodynamic benefits may have been gained as the patient?s cardiac output appeared to increase and improve gradually after his placement on HFOV. This case may show that HFOV could be used in a proactive role in the correct patient population as opposed to the rescue mode usually used today.