Fluid therapy for critically ill, hemodynamically selleck chemical unstable patients presents clinicians with a dilemma. On the one hand, a fluid bolus may augment cardiac output, improve critical organ perfusion, and even save the patient’s life. On the other hand, fluid may confer no hemodynamic benefit, while adding to pulmonary edema, amongst other ills. How often is a fluid bolus harmful, as opposed to helpful? When an intensivist judges that a fluid bolus is necessary, only one-half of patients respond with a meaningful boost in cardiac output [2]. Especially for patients most likely to be harmed (for example, those with concomitant acute lung and kidney injury), knowing whether fluids will enhance perfusion should be clinically valuable.

Historically, clinicians have relied on static hemodynamic parameters, such as the central venous pressure, to judge whether fluids are likely to aid the circulation. A multitude of studies, accumulating for more than two decades, show that the central venous pressure and its more invasive cousin, the pulmonary artery occlusion (or wedge) pressure, are no more reliable than a coin toss in forecasting whether an individual subject will respond positively to a fluid bolus. When seen in subjects with sepsis [3], with acute respiratory failure [4], or following cardiac surgery [5], this lack of predictive accuracy was attributed to effects of surgery or positive end-expiratory pressure on, for example, ventricular compliance.

How disturbing, then, to find that the central venous pressure and pulmonary artery occlusion pressure fail to correlate with ventricular volumes or fluid responsiveness even in healthy normal individuals [6]!In contrast to the failure of static measures, a novel set of predictors that rely on perturbing the circulation accurately foretell whether fluids will augment cardiac output. These dynamic measures generally employ controlled mechanical ventilation to raise the pleural pressure (some alternatively depend on raising the legs, measuring the effect of spontaneous breathing, or altering the positive end-expiratory pressure) and quite accurately predict fluid responsiveness. In the passive patient, the stroke volume varies with ventilation to a degree that reflects whether the ventricles are operating on the rising or flat portion of the Starling function curve. Patients whose circulations can respond Batimastat to fluids will therefore demonstrate substantially greater cyclical variability in stroke volume. As the stroke volume changes, so vary the systolic pressure [7], the pulse pressure [7], and the aortic blood flow velocity [8]. Similar cardiopulmonary interactions explain that changes in the diameter of the inferior vena cava also predict fluid responsiveness [9,10].