Our study shows that, irrespective of baseline values, an increase of 2% or more in SvO2 during fluid loading for clinical hypovolemia after cardiac or major vascular surgery indicates fluid responsiveness of the heart, in spite of concomitant hemodilution and a rise in VO2I tending to lower SvO2[11–15, 17]. The value is greatest when baseline systolic cardiac function and thus SvO2 are relatively low, since the percentual increase in CI in the steep part of the cardiac function curve may increase when the latter is displaced downward and to the right.
The patient’s need for fluid loading was judged on clinical grounds and not all patients responded to fluid loading, confirming the superiority of hemodynamic over clinical judgement and the relatively poor predictive value, even at low PEEP, of filling pressures in this respect
[6, 8]. Our data also suggest that fluid non-responsiveness was not primarily caused by pulmonary hypertension and right ventricular overload, since MPAP never reached values above 35 mm Hg after fluid loading. However, MPAP was slightly higher in patients with low vs normal GEF at baseline, so that increased right ventricular afterload and dysfunction cannot be excluded to have contributed to relatively high GEDVI and non-response to fluids. Also, we cannot exclude a higher left ventricular afterload with higher MAP contributing to a low GEF and cardiac dilatation in some of our patients. The monitoring value of increases in SvO2 is otherwise similar to that of GEDVI, suggesting that the pulmonary artery catheter and the transpulmonary dilution technique are of similar value in assessing fluid responsiveness, by allowing CI measurements as well as direct indicators of tissue oxygenation and preload reserve, respectively. Insertion of a femoral artery catheter is sometimes considered less invasive than that of a pulmonary artery catheter, however, and the transpulmonary technique also allows monitoring of dynamic indices, which may be of value under some circumstances. In favour of the pulmonary artery catheter on the other hand is the possibility of continuous monitoring of SvO2 to guide and assess fluid therapy in intervals that arterial O2 saturation, haemoglobin and VO2I can be assumed to be unchanged
[9–15, 19]. Moreover, mathematical coupling if variables are taken from the same dilution curves may argue against the seeming superiority (and higher correlation) of GEDVI over SvO2 increases to reflect CI increases with fluid loading
. In contrast, pulmonary catheter-derived CI and SvO2, measured independently of each other, are not mathematically coupled.
Our finding that an increase in SvO2 can be used as a monitor of fluid responsiveness in cardiac patients is supported by Giraud et al.
. We found that an increase in SvO2 by 2% or more indicates fluid responsiveness, whereas they
 found a threshold of 7%. Their baseline SvO2 was lower than ours, thereby increasing the rise in SvO2 for a given rise in CI, because of the curvilinear relation between SvO2 and CI, so that changes in relatively high SvO2 are less, for given changes in (relatively high) CI, than at low SvO2 (and thus low CI)
[11, 12, 18]. As in our study, Inomata et al.
 found a positive correlation between increases in SvO2 and CI measured with help of a fibreoptic pulmonary artery catheter. However, they studied patients during cardiac surgery and did not specifically look at fluid responses. They observed that when baseline CI was less than 2 L/min/m2 the correlation with SvO2 was better than when it was above 2 L/min/m2, probably because the SvO2 was lower with the former. The effect may be caused, again, by the curvilinear relation between CI and SvO2 at unchanged arterial O2 saturation, hemoglobin and VO2I
[11, 12, 18]. This may also explain, together with relatively large fluid responses, the seemingly greater value of an increase in SvO2 to reflect fluid responsiveness, when baseline cardiac function and thus SvO2 are relatively low in our study.
In contrast to our observations, Viale et al.
[13, 15] found no correlation between CI and SvO2 in the three first postoperative hours after aortic surgery, although they found a positive correlation during surgery. They concluded that lack of correlation was due to a concomitant increase in VO2I, that peaked in de second postoperative hour and then returned to preoperative values. Our study started within three hours of arrival at the ICU, and therefore O2 needs may have stabilized, although we cannot exclude that supply-dependent VO2I attenuated the increase in SvO2 with fluid loading in responders, given the inverse correlation between VO2I and SvO2 changes. Otherwise the concomitant increase in DO2I and VO2I can be partly explained by mathematical coupling, in the absence of changes in SvO2. The baseline SvO2 was >70% in many of our patients, and the lactate levels were near normal, particularly in non-responders, and this could together indicate adequacy of tissue oxygenation
[1–3, 11, 12, 18, 19]. Indeed, the similar baseline VO2I among responders and non-responders may indicate similar tissue oxygen needs. The VO2I increased with fluid loading in the whole group, but we cannot exclude that this related to increased work performed by the heart following an increased MAP and thus stroke work, even at unchanged CI in non-responders, rather than improved peripheral tissue oxygenation. The lactate levels marginally increased in low GEF patients, possibly consistent with lowered oxygen supply to demand to the heart. In the recent study by Monnet et al.
 neither baseline nor changes in ScvO2 were associated with fluid responsiveness, but this may partly relate to ScvO2 being a poor measure of SvO2 in their predominantly septic patients, also mostly displaying DO2-dependent VO2. In agreement with our study, however, the DO2 increased in fluid responders
. Our results may not be extrapolated to changes in ScvO2, which may be confounded by changes in mixing of blood from caval veins and coronary sinus
This study carries limitations. We only studied patients after cardiac and vascular surgery and the results may not apply to septic or trauma patients. This study was not designed to improve patient outcomes but to study the circulatory effects of fluid loading, in a posthoc analysis. SvO2 measurements still require a pulmonary artery catheter and we cannot judge the relative value of ScvO2 monitoring via central venous catheters, although large differences between the two measurements have been reported after cardiac surgery
[10–12, 17, 20]. The data also suggest that predictive values were independent of the type of fluid loading applied. Finally, the data indicate that responders and non-responders differed in their position on the cardiac function curve, regardless of GEF and position of the curve. The difference is also unlikely caused by an accidental and overall borderline significant difference of 10%, at maximum, in fluid volume load that otherwise exceeded 1 L. The difference may have been evoked by our fluid algorithm limiting fluids when filling pressures increase by more than 5–7 mm Hg
 per 10 min potentially affecting non-responders more than responders.