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In anesthetized patients without cardiac arrhythmia the arterial pulse pressure variation (PPV) induced by mechanical ventilation has been shown the most accurate predictor of fluid responsiveness. In this respect, PPV has so far been used mainly in the decision-making process regarding volume expansion in patients with shock. As an indicator of the position on the Frank-Starling curve, PPV may actually be useful in many other clinical situations. In patients with acute lung injury or with acute respiratory distress syndrome, PPV can predict hemodynamic instability induced by positive end-expiratory pressure and recruitment maneuvers. PPV may also be useful to prevent excessive fluid restriction/depletion in patients with pulmonary edema, and to prevent excessive ultrafiltration in critically ill patients undergoing hemodialysis or hemofiltration. In the operating room, a goal-directed fluid therapy based on PPV monitoring has the potential to improve the outcome of patients undergoing high-risk surgery.In the previous issue of Critical Care, Keyl and colleagues [1] have investigated the effects of cardiac resynchronization therapy on arterial pulse pressure variation (PPV). Many studies [2] have shown that PPV is much more accurate than cardiac filling pressures and volumetric markers of preload to predict fluid responsiveness (that is, the hemodynamic effects of volume loading). PPV is also more reliable than other dynamic parameters such as systolic pressure variation [3,4] or pulse contour stroke volume variation [4]. In this respect, PPV is used increasingly in the decision-making process regarding volume expansion in patients with hemodynamic instability [2]. Limitations to the use of PPV do exist (mainly active breathing, cardiac arrhythmia, and low tidal volume) and have been described in detail elsewhere [2,5].It is very important to point out that PPV is not an indicator of volume status, nor a marker of cardiac preload, but is an indicator of the position on the Frank-Starling curve [2].Briefly, patients operating on the flat portion of the Frank-Starling curve are insensitive to cyclic changes in preload induced by mechanical inspiration, such that PPV is low (Figure 1). Conversely, PPV is high in patients operating on the steep portion of the preload/stroke volume relationship (and hence sensitive to cyclic changes in preload induced by mechanical inspiration) (Figure 1). This information has so far been used mainly to predict fluid responsiveness in patients with shock, but actually could be useful in many other clinical situations. PPV and fluid depletion/restrictionAs an indicator of the position on the Frank-Starling curve, PPV is as useful to predict the deleterious hemodynamic effects of fluid depletion as it is to predict the beneficial effects of fluid loading [6]. In critically ill patients undergoing hemodialysis or hemofiltration the volume of ultrafiltration is often determined roughly on the basis of body weight gain or fluid balance, and is further adjusted in case of hemodynam...

Background:  Pulse pressure variation (ΔPP) and systolic pressure variation (SPV) induced by mechanical ventilation have been proposed to detect hypovolaemia and guide fluid therapy. During laparoscopic surgery, chest compliance is decreased by pneumoperitoneum. This may affect the value of SPV and ΔPP as indicators of intravascular volume status. Thereby, we investigated the effects of pneumoperitoneum and hypovolaemia on SPV and ΔPP.Methods:  We measured ΔPP, SPV and the inspiratory (Δup) and expiratory (Δdown) components of SPV, at baseline, during pneumoperitoneum, during pneumoperitoneum and hypovolaemia and after the return to baseline conditions, in 11 mechanically ventilated rabbits. Pneumoperitoneum was induced by inflating the abdomen with carbon dioxide, and hypovolaemia was induced by controlled haemorrhage.Results:  Pneumoperitoneum induced an increase in SPV from 8.5 ± 1.6 to 13.3 ± 2.6 mmHg (+56%, P < 0.05) as a result of an increase in Δup from 2.0 ± 1.0 to 6.7 ± 2.1 mmHg (+236%, P < 0.05), but no significant change in Δdown, nor in ΔPP. Haemorrhage induced a significant (P < 0.05) increase in SPV from 13.3 ± 2.6 to 19.9 ± 3.7 mmHg (+50%), in Δdown from 6.6 ± 3.3 to 14.0 ± 4.9 mmHg (+112%) and in ΔPP from 11.1 ± 4.8 to 24.9 ± 9.8% (+124%) but no change in Δup. All parameters returned to baseline values after blood re‐infusion and abdominal deflation.Conclusions:  SPV is modified by haemorrhage but it is also influenced by pneumoperitoneum. In contrast, ΔPP is modified by haemorrhage but not by pneumoperitoneum. These findings suggest that ΔPP should be used preferentially instead of SPV to detect hypovolaemia and guide fluid therapy during laparoscopic surgery.