Some light in the grey zone?

Treatment of shock is not a new concern in intensive care medicine. The highest priority in patients with shock is the restoration of oxygen delivery. Fluid resuscitation is the very first goal of increasing cardiac output and oxygen delivery in patients with acute circulatory insufficiency. First, based on the simple physiology of the Frank–Starling mechanism, fluid loading should increase cardiac output (CO) by increasing preload and subsequently increasing left ventricular (LV) stroke volume.¹ However, fluid overload, especially in patients with pre-existing or developing cardiac failure, can end in only a fractional increase of stroke volume and negative effects like pulmonary venous congestion can predominate. It is therefore a daily task for each intensivist to identify those patients who will respond to and benefit from volume expansion (e.g. acute shock) and to avoid fluid overload in those who are no longer fluid responsive but are at risk for increased mortality by further fluid therapy (e.g. protracted sepsis, acute respiratory distress syndrome, acute kidney injury). Thus the therapeutic conflict between hypovolaemia and hypervolaemia needs to be addressed wisely. Consequently, precise monitoring of preload could be helpful in this clinical scenario (Fig. 1).

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