Extravascular fluids

Diffusible plasma / tissue / extravascular fluid / red blood cells / bound plasma (x103) / urinary bladder / urinary path /small intestine /trabecular bone surface / cortical bone surface / liver, rapid turnover rate / other kidney (x103) / other soft tissues, rapid turnover rate / other soft tissues, moderate turnover rate (x10) / other soft tissues, slow turnover rate (x102) / brain (x103) / sweat Bone / tissue (x103) 1,000 297-480 500-800 19-30 25-40 7.4-12.0 58-132 71-384 50-80 350-400 103-178 100-178 124-200 188-763 4.3-7.0... 

Kihara, T. (1950). The extravascular fluid passway system. Ketsuekigaku Togikai Hokoku 3 118 cited in Nagaishi (1972). 

Distribution - IV or subcutaneous administration distributes mainly in blood and only to a minor extent in extravascular fluid. Apparent volume of distribution is 7 to 11 L. Fondaparinux is highly (at least 94%) and specifically bound to ATIII. 

Pharmacokinetics Distributed mainly in blood and to some extent in extravascular fluid. Iron sucrose is dissociated into iron and sucrose by the reticuloendothelial system. The sucrose component is eliminated mainlyby urinary excretion. Haif-life 6 hr. 

The primary function of lipoproteins is to transport insoluble lipids through the aqueous environment of the vascular and extravascular fluids, and the relative... 

In many diseases the amount of sodium chloride reabsorbed by the kidney tubules is abnormally high. This leads to the retention of water, an increase in blood volume, and expansion of the extravascular fluid compartment, resulting in edema of the tissues. Several commonly encountered causes of edema include ... 

CME results from many ocular conditions but is not an independent disease entity. Retinal cell processes in Henle s layer run parallel to the surface of the internal limiting membrane, and the laxity of this layer fc>rms a potential reservoir for extravascular fluid resulting from breakdown of the blood-retinal barrier, which forms extracellular cystoid spaces in the perifoveal area. CME accompanies several retinal vascular diseases, including diabetic maculopathy central retinal venous occlusion, and branch venous occlusion. It may follow surgical procedures, most often cataract extraction and retinal detachment repair, or posterior inflammatory conditions, including pars planitis, chronic uveitis, and miscellaneous conditions such as retinitis pigmentosa. 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

Renal toxicity has been attributed to sequelae from the development of the capillary leak syndrome. Vascular leak resulted in significant extravascular fluid accumulation (ascites, pleural effusions, peripheral edema) and weight gains of as much as 17 kg in 3 weeks [11]. As in sepsis syndrome, hypotension, oliguria and reduced fractional excretion of sodium accompanied the capillary leak. 

The rehydration phase aims to replace extravascular fluid losses. Crystalloid fluids are a logical choice for rehydration as they readily diffuse into the interstitial fluid from the vasculature (Spalding Goodwin 1999, Vaupshas Levy 1990). Rehydration should take place over the first 12-24 h of therapy. The amount given should be based on the clinical estimate of the degree of dehydration and the response to fluid therapy. 

In patients with edema or ascites associated with low plasma albumin, the effect of albumin infusion is very transient because of rapid equilibration with the extravascular fluid. The only situation in which infusion is usually beneficial is in acute hypovolemic shock in this case, rapid infusion may result in hypocalcemic tetany, because albumin binds Ca " with relatively high affinity. 

Plasma protein concentrations are dynamic parameters that depend on the biosynthesis, distribution between intravascular and extravascular fluid compartments, and elimination (degradation, catabolism, and loss) of the proteins. Table 8.3 lists some of the common causes for changes of plasma protein and albumin concentrations. A rise in plasma albumin is often due to dehydration, and this can be confirmed by associated increases of plasma globulins, blood hemoglobin, and hematocrit (packed cell volume). 

Shock may be caused by myocardial, intestinal, or brain infarction, hyperthermia, tachyarrhythmias, or hypovolemia produced by extravascular fluid sequestration owing to vasoconstriction. 

The hemoglobin level is not a specific marker of hemorrhage as, in the acute stages, the hemoglobin or hematocrit is likely to be normal. A few hours are required before extravascular fluids equilibrate with the blood and for laboratory values to reflect blood loss. It is imperative to obtain two intravenous accesses with large bore cannulas and start an infusion of intravenous fluids as soon as possible. 0-negative blood should be readily available, and blood samples should be sent early for cross matching. 

Kappagoda, C. T. and K. Ravi. 2006. The rapidly adapting receptors in mammalian airways and their responses to changes in extravascular fluid volume. Experiment Physiol 91 647-54. 

---