Fluid Therapy in Septic Shock

  • L. G. Thijs
Part of the Update in Intensive Care and Emergency Medicine book series (UICM, volume 19)


In patients with septic shock, hypovolemia is a major factor contributing to circulatory instability. In the early phase, cardiac filling pressures are often lowered, due to a decrease in venous return, compromising cardiac output and tissue perfusion [1, 2]. A decline in effective circulating volume can be induced by a variety of sepsis-related mechanisms. First, generalized vasodilation increases total vascular capacitance with subsequent relative hypovolemia. A decline in systemic vascular resistance, mainly due to arteriolar vasodilation, is a constant feature in human septic shock [3]. Alterations in the venous capacitance system, by far the largest part of the intravascular compartment, are however difficult to assess. The concept of venous pooling as a major factor limiting effective venous return stems from animal experiments [4, 5]. Experimental studies in endotoxin and sepsis models have indicated that in several body areas venous capacitance increases. Although significant increases in venous capacitance in the forearm could not be demonstrated in the clinical study [6], it is likely that also in human septic shock venous pooling in vascular beds other than skeletal muscle (e.g. the splanchnic area) is an important mechanism. The evidence for this is, however, only circumstantial. The observation that large amounts of fluids are usually required for initial resuscitation supports such a concept. Secondly, absolute hypovolemia may contribute to a defect in effective circulating volume. This could be due to fever with perspiration and increased insensible loss, vomiting, diarrhea, volume loss by drains or sequestration (e.g. in the gut), and inadequate oral intake.


Septic Shock Pulmonary Edema Fluid Therapy Extravascular Lung Water Circ Shock 
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