Pathophysiology of fluid imbalance

Uwe Kreimeier

doi:10.1186/cc968

Abstract

Fluid imbalance can arise due to hypovolemia, normovolemia with maldistribution of fluid, and hypervolemia. Trauma is among the most frequent causes of hypovolemia, with its often profuse attendant blood loss. Another common cause is dehydration, which primarily entails loss of plasma rather than whole blood. The consequences of hypovolemia include reduction in circulating blood volume, lower venous return and, in profound cases, arterial hypotension. Myocardial failure may result from increased myocardial oxygen demand in conjunction with reduced tissue perfusion. Finally, anerobic metabolism due to reduced perfusion may produce acidosis and, together with myocardial dysfunction, precipitate multi-organ failure. The splanchnic organs are particularly susceptible to the deleterious effects of hypotension and hypovolemic shock, and these effects, depending upon their duration and severity, may be irreversible despite restoration of normovolemia by fluid administration. Patient monitoring in the intensive care unit typically relies upon central venous pressure devices, whereas the primary focus in the operating theater is blood volume deficit estimated from suction devices. However, estimates of intraoperative blood loss can be inaccurate, potentially leading to inappropriate fluid management. Normovolemia with maldistribution of fluid can be encountered in shock-specific microcirculatory disorders secondary to hypovolemia, as well as pain and stress. Consequent vasoconstriction and reduced tissue driving pressure, as well as leukocyte and platelet adhesion, and liberation of humoral and cellular mediators, may impair or abolish blood flow in certain areas. The localized perfusion deficit may contribute to multi-organ failure. Choice of resuscitation fluid may be important in this context, since some evidence suggests that at least certain colloids might be helpful in diminishing post-ischemic microvascular leukocyte adherence. Excessive volume administration may lead to fluid overload and associated impairment of pulmonary function. However, entry of fluid into the lungs may also be facilitated by increased vascular permeability in certain pathologic conditions, especially sepsis and endotoxemia, even in the absence of substantially rising hydrostatic pressure. Another condition associated with elevated vascular permeability is systemic capillary leak syndrome. The chief goal of fluid management, based upon current understanding of the pathophysiology of fluid imbalance, should be to ensure adequate oxygen delivery by optimizing blood oxygenation, perfusion pressure, and circulating volume.

Highlights

A discussion of the pathophysiology of fluid imbalance typically focuses on hypovolemia
What precepts of fluid management emerge from current understanding of the pathophysiology of fluid imbalance? The fundamental requirement of the patient is oxygen, and sufficient oxygen delivery is a paramount goal of fluid management that can be attained by ensuring adequate pulmonary function
Another important goal is satisfactory perfusion pressure, which depends upon myocardial performance and vascular tone

Summary

Introduction

A discussion of the pathophysiology of fluid imbalance typically focuses on hypovolemia. Notwithstanding apparent normovolemia and the re-establishment of normal blood pressure and cardiac output after appropriate therapeutic interventions such as fluid administration, localized perfusion may be inadequate or nonexistent, and multi-organ failure may ensue. Fluid extravasation leads to hematocrit increases of 70% or more, placing the patient at risk for thrombosis Another feature of SCLS is secondary hyperaldosteronism, and the condition is associated with monoclonal gammopathy. A rise in lung microvascular pressure greater than two-fold was required in the absence of administered endotoxin to increase lung lymph flow two-fold It remains clear, without regard to the extent of vascular permeability, that administration of sufficiently large volumes can in itself result in fluid overload to tissues, and the lung and gut are primarily affected. Permissive hypotension might, depending upon the extent of reduced blood pressure, lead to a clinically undesirable enhancement of neutrophil adhesion

Conclusion

Findings

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