Of critically ill patients with conventional indications for a fluid bolus, only about half will respond with a meaningful increase in perfusion.
Fluid therapy that does not boost perfusion may cause harm by impairing lung function, producing edema in other organs, or contributing to endothelial dysfunction.
Static hemodynamic parameters, such as central venous pressure or pulmonary artery occlusion pressure, have little value in guiding fluid therapy.
Fluid responsiveness can be predicted using cardiopulmonary interactions to probe circulatory function or through passive leg raising.
Dynamic fluid-responsiveness predictors are accurate but require careful attention to preconditions for validity.
Critical illness often cripples the circulation. For example, septic shock combines ventricular dysfunction; arteriolar dilation; vascular obstruction; and volume depletion due to transudation of fluid from the vascular space into tissues, venodilation, reduced oral intake, and heightened insensible loss. Trauma produces similar effects through hemorrhage, spinal injury, cardiac tamponade, tension pneumothorax, acidemia, and cardiac dysfunction. These join to compromise perfusion globally, threatening the function of vital organs. Urgent resuscitation improves outcome in shock, showing that time is of the essence, a concept captured in the phrase “the golden hour.”1,2 Treating hypovolemia has been a central tenet of shock management. Nevertheless, many controversies remain regarding the details of shock resuscitation, including the role and type of fluid therapy, metrics for assessing the response, and clinical end-points.
Initial resuscitation transforms a hypovolemic, hypodynamic circulation into one where oxygen transport is normal or high, at least at the whole body level, in most septic adults2,3 and even following trauma and cardiac arrest.4 In contrast to the average patient entering the early goal-directed trial,2 once fluids, antimicrobials, vasoactive drugs, and perhaps blood have been given, resuscitated patients typically display elevated central venous pressure (CVP), cardiac output, and mixed and central venous oxyhemoglobin saturations (SvO2 and ScvO2, respectively). There is no longer global hypoperfusion as judged by most measures of oxygen transport, even when hypotension, lactic acidosis, and organ dysfunction persist. Nevertheless, the macrocirculation remains grossly impaired and mean arterial pressure is rarely restored to normal.
Indeed, persistent hypotension and progressive organ failures often prompt further fluid administration. When given additional fluid, some patients will respond: blood pressure, cardiac output, oxygen delivery, ScvO2, or urine output increases. Other patients will not hemodynamics fail to improve, and the fluid bolus is ineffective at best.5 Moreover, ineffective fluid challenges often lead to additional boluses, culminating in a grossly edematous patient (still hypotensive and oliguric). In one prospective study of fluid boluses in septic patients, fluid boluses constituted 50% of fluid gain on day 1 and roughly 30% on days 2 and 3.6 Even a positive initial response is only sustained at 30 minutes in half of “responders.”7 These findings fundamentally call into question the prominent role for fluid therapy in shock.8...