Author’s reply to the comment by Dr. Bendjelid

Excerpt

Sir: We thank Dr. Bendjelid [1] for his interesting remarks regarding our recent contribution to Intensive Care Medicine. He gives us the opportunity to correct some misinterpretations. We did not report that “dynamic indices” are not reliable predictors of fluid responsiveness in patients with high right ventricular impedance. We merely pointed out that under certain conditions such as severe acute cor pulmonale, significant variations in pulse pressure may be observed without reflecting fluid responsiveness [2]. We do not agree when Dr. Bendjelid suggests that a possible explanation of this phenomenon is a decrease in systemic venous return related to tidal ventilation, which could thus decompress the overdistended right ventricle (RV) and so induce an improvement in left ventricular filling. We think rather that this is induced by an inspiratory increase in RV impedance, leading to increase in RV overload. Indeed we never observed a decrease in RV size at inspiration, which is expected in the case of RV “decompression,” whereas we previously reported a clear inspiratory increase in RV end-diastolic and end-systolic area [3]. In all cases, in this situation, we can indeed imagine an inspiratory increase in inferior vena cava (IVC) diameter, leading to significant respiratory variations in IVC diameter, but without reflecting a fluid responsiveness state. However, variations in IVC diameter depend not only on the amount of blood contained in the vessel but also on the compliance of the vessel which is markedly decreased in conditions of overdistention. This is illustrated in the Fig. 1, using unpublished data of our team concerning the correlation between IVC diameter and central venous pressure (CVP). From a certain diameter (greater than 20 mm) the IVC is not able to dilate any more because it currently remains on the horizontal part on its pressure-diameter relationship. In a study of patients with acute respiratory distress syndrome our group demonstrated that IVC is markedly dilated in the patients with severe acute cor pulmonale, suggesting the impossibility of further significant dilation [4].

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