Assessment of volume responsiveness during mechanical ventilation: recent advances

Predicting which patients with acute circulatory failure will respond to fl uid by a signifi cant increase in cardiac output is a daily challenge, in particular in the setting of the intensive care unit (ICU). Th is challenge has become even more crucial because evidence is growing that administering excessive amounts of fl uid is a risk factor in critically ill patients, in particular in patients with lung injury. However, some tests and indices allow prediction of fl uid responsiveness before intravenous fl uids are infused. In patients receiving mechanical ventilation, the arterial pulse pressure variation (PPV) has been used for many years. More recently, other tests, which may overcome some limitations of PPV, have been developed. In addition, recent studies have emphasized how the hemo-dynamic eff ects of volume expansion should be assessed once fl uid has been administered. Volume expansion is the fi rst-line treatment in the majority of cases of acute circulatory failure. Fluid is administered with the expectation that it will increase cardiac preload and cardiac output to a signifi cant extent. Nevertheless, this can occur only if cardiac output is dependent upon cardiac preload, i. e., if both ventricles operate on the ascending limb of the cardiac function curve [1] (Fig. 1). If this is not the case, volume expansion may only exert adver se eff ects without having any hemodynamic benefi t. An important point is that excessive fl uid administration has been demonstrated to increase mortality during septic shock [2,3] and to prolong mechanical ventilation during acute respiratory distress syn dr ome (ARDS) [4]. In the same co ntext, the amount of extravascular lung water (EVLW), i. e., the volume of lung edema, has been demonstrated to be related to mortality in critically ill patients [5] and, more recently, to be an independent prognostic factor during ARDS [6]. Th us, fl uid responsiveness should be detected before deciding to administer volume expansion, especial ly in patients in whom fl uid overload should be particularly avoided, i. e., patients with septic shock and/ or ARDS. For this purpose, 'static' markers of cardiac preload have been used for many years. Nevertheless, a very large number of studies clearly demonstrate that neither pressure nor volume markers of preload can predict fl uid responsiveness [7,8]. Th is fi ndin g is mainly because a given value of preload can correspond to either a large or a negligible …