Abstract 160: Impact of Myocardial Dysfunction on Fluid Responsiveness After Resuscitation from Cardiac Arrest
Background: Fluid therapy for hemodynamic stabilization after CA is challenging. Therefore, predicting fluid responsiveness is an important issue. We recently showed that transesophageal echocardiography (TEE) may provide helpful information whether stroke volume will increase after fluid loading [1, 2]. The aim of the present study was to evaluate the impact of post-CA myocardial dysfunction on the performance of TEE to predict fluid responsiveness.
Methods: After IRB approval, electrically induced CA of 8 minutes was followed by CPR in 25 anesthetized pigs. TEE derived respiratory variation of velocity time integral (ΔVTI) and variation of aortic blood velocity (ΔVpeak) were measured before and after a 5 ml/kg fluid load at BL, and 2, 3, and 4 hours after ROSC. Animals with an increase in stroke volume of at least 15% after fluid loading were classified as responders, otherwise as non-responders. Ejection fraction (EF) was determined using mid-esophageal long-axis view. Considering a threshold EF of 50%, performance of variables were analyzed using receiver-operator characteristics (ROC) calculating the area under the curve (AUC) for low (<50%) and normal EF.
Results: Decreased EF was significantly associated with decreased stroke volume (p<0.01) and increased heart rate (p<0.01) after ROSC. At BL, variables enabled prediction of fluid responsiveness (ΔVTI: AUC=0.72, p<0.05; ΔVpeak: 0.76, p<0.01). After ROSC, however, prediction of fluid responsiveness was impaired when EF was < 50% (ΔVTI: 0.55, p=0.68; ΔVpeak: 0.57, p=0.54) but not if EF was > 50% (ΔVTI: 0.84, p<0.01; ΔVpeak: 0.73, p<0.05; Fig. 1).
Conclusion: The present study indicates that myocardial dysfunction may impair prediction of fluid responsiveness by TEE. Therefore, implementation of these variables into protocols for hemodynamic optimization should consider these limitations.
References: 1. Feissel M et al. Chest (2001) 119:867, 2. Gruenewald M et al Circulation (2010) ReSS Poster 182
- © 2011 by American Heart Association, Inc.