A COURAGOUS CALL: SALINE FOR HEART FAILURE? M. Guidry 1 , J. Wiese 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77054) LEARNING OBJECTIVES: 1. Recognize the perils of over-diuresis in bi-ventricular heart failure. 2. Use disciplined methods of diagnosis to prevent errors in pattern recognition diagnosis. 3. Use the physical examination to predict cardiovascular function. CASE INFORMATION: An 80 year-old woman presented with two days of shortness of breath and orthopnea. Her blood pressure was 132/65 with a heart rate of 116. She had bibasilar crackles and 3+ pitting bipedal edema. There was an S3, S4, and an inferiorly displaced PMI. Her room-air ABG at presentation was pH: 7.44; pCO2:35; pO2:58. She was diuresed with a total of 320 mg of furosemide over one day. Her symptoms improved. On the third hospital day, she had a sudden worsening of her shortness of breath. Her neck veins were flat and there were no crackles. A repeat ABG was pH: 7.28; pC02: 57; p02: 81; HCO3:42 Her BUN tocreatinine ratio increased from 23/1.4 at presentation to 41/2.3 on the third hospital day. Diuresis was stopped, and hydration with normal saline was initiated. Her shortness of breath improved, with normalization of her acid base values. IMPLICATIONS/DISCUSSION: Dyspnea can result from hypoxia or hypercarbia. This patient initially presented with dyspnea due to congestive heart failure; she was appropriately managed with preload reduction via diuresis. Continuing diuresis was excessive however. In the setting of bi-ventricular heart failure, the over-diuresis resulted in an inadequate right ventricular preload, and a subsequent drop in her pulmonary artery pressure. With the alveolar pressure unchanged and the pulmonary artery pressure lowered, the percentage of dead space increased. This resulted in a ventilation to perfusion mismatch resulting in hypercarbia. The physical examination was the tell-tale sign, revealing that her volume status was low, instead of high. The ABG confirmed the diagnosis; the rehydration increased the pulmonary artery pressure, resolving the mismatch, and eliminating the dyspnea. In caring for patients with biventricular heart failure who are sensitive to preload reduction, it is important to remember that hypercarbia from dead space ventilation can result from aggressive lowering of the pulmonary artery pressure.