Dynamic variables of fluid responsiveness such as pulse pressure variation (PPV) and stroke volume variation (SVV) have been shown to reliably predict the response to fluid administration in different patient populations. The influence of increased intra-abdominal pressure (IAP) on the predictive ability of these variables is currently under debate. Therefore, the present study was designed to evaluate whether PPV and SVV are suitable for predicting fluid responsiveness during elevated IAP.
Prospective controlled experimental study.
Animal research laboratory.
14 anesthetized and mechanically ventilated pigs.
Pigs were studied at different experimental stages: normovolemia at baseline conditions, after induction of pneumoperitoneum (PP) by increasing IAP up to 25 mm Hg, followed by releasing PP and performing a fluid load with 1000 cc hydroxyl-ethyl starch 6%, and finally after inducing PP again. Cardiac output, stroke volume, central venous pressure, and pulmonary artery occlusion pressure were obtained by pulmonary artery thermodilution. Additionally, global end-diastolic volume (GEDV) was measured by transpulmonary thermodilution. PPV and SVV were monitored continuously by pulse contour analysis.
PP induced significant changes in peak airway pressure, esophageal pressure, chest wall compliance, SVV, PPV, central venous pressure, and pulmonary artery occlusion pressure independent of loading conditions. As assessed by receiver operating characteristic curve analysis, PPV, SVV, and GEDV accurately predicted fluid responsiveness before IAP was increased (area under the curve: 0.90, 0.91 and 0.91). A PPV value of ≥11.5%, a SVV value of ≥9.5%, and a GEDV value of ≤963 mL accurately predicted an increase in stroke volume ≥15%. After increasing IAP, the ability of SVV to predict fluid responsiveness was abolished, whereas it was preserved with both PPV and GEDV, although the threshold value for PPV dramatically increased up to ≥20.5%.
In this animal model PPV and GEDV proved to be sensitive and specific predictors of fluid responsiveness even during increased IAP.
From the Department of Anaesthesiology and Intensive Care Medicine (JR, MG, RH, PM, MS, JS, BB); and Department of Cardiothoracic and Vascular Surgery (RQ), University Hospital Schleswig-Holstein, Campus Kiel, Germany.
The authors have not disclosed any potential conflicts of interest.
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