The question, as always, is "can I give this guy more fluid?" For any given patient, there will be some sort of unique and magical volume which represents their ideal ventricular filling volume. Achieving this ideal volume results in the greatest contractility improvement and the highest cardiac output for this specific patient.
However, what this magical volume value is - that is a guess at best. We have no real way of measuring the ventricular end-diastolic volume anyway- we only have substandard measures. Back in the day, we would have used PAWP as a surrogate measure of LA pressure, which in turn is a surrogate measure of LV filling pressure, which in turn is an imperfect surrogate measure of LV filling volume. This string of inferences is fraught with error, and in any case nobody uses PA catheters routinely these days. Well, apparently 68% of you still do, but at least nobody still uses the PAWP as a measure of preload anymore. Nevermind: if you do find yourself trapped in the land of PAWP-directed preload management, remember that the post-cardiotomy patient with their decreased ventricular compliance will need a higher filling pressure to achieve a given volume, and thus one may wish to run these people at a slightly higher PAWP. All the while remembering that PAWP is almost completely disconnected from preload.
The manufacturers of advanced hemodynamic monitoring devices produce papers which would have us believe that their equipment can inform our use of fluids and thereby decrease the post-operative use of vasopressors and inotropes. Particularly, the GEDV is a calculated variable which has been widely trumpeted as a good number to base one's fluid management upon. One gives fluid challenges to increase the GEDV, and one stops either when they fail to increase the GEDV or the EVLWI increases, demonstrating that one has now flooded the lungs. Of course, as with all device-directed physiological manipulation, its a game of numbers and at no stage is anyone actually invited to look at the patient and assess their condition. Additionally, GEDV does not seem to stand up well in meta-analysis - its seems to be as bad as PAWP and CVP.
So, the enraged pragmatist might snarl "so what the hell do we use to assess preload?" and more directly "how the devil am I supposed to decide whether more fluids will help my cardiac output?"
For this, I refer to an article by Marik, which in 2010 nicely summarised the physiology behind the various bedside tests we use to assess fluid responsiveness. This not specific to post-bypass patients and as a general topic is dealt with elsewhere. In the interest of link economy, I will summarise the most important points here:
Though fluid responsiveness is a rather attractive topic, it is equally important to understand that increased preload is also a terrible problem. Contractility will suffer if the ventricle is over distended. Vasodilators, particularly venodilators such as GTN and sodium nitroprusside, are the natural choice for the management of this problem.