As an exercise in applied fluid physiology is to compare the distribution and excretion of a rapid intravenous infusion of 1000 mls of various fluids. This serves to emphasise some of the factors involved in the selection of an appropriate fluid. In this exercise we will tend to ignore cardiovascular changes such as increased venous capacitance.

Certain simplifing assumptions are made in clinical practice about the sizes of the various fluid compartments to facilitate the mental arithmetic without loss of any clinically relevant precision. The water of dense connective tissue & bone is significant in volume (15% of total body water) but as a kinetically slow compartment. It is not important in consideration of short term fluid distribution. Transcellular fluids are small in volume and usually slow so they too are excluded from this clinical analysis.

This leaves three big compartments:

Dextrose 5% is a ‘Maintenance Fluid’. (Dextrose is d-glucose). It is isosmotic as administered and does not cause haemolysis. The glucose is rapidly taken up by cells. The net effect is of administering pure water, so it is distributed throughout the total body water. Each compartment receives fluid in proportion to its contribution to the TBW (ie 2/3rd to ICF and 1/3rd to ECF; the ECF fluid is distributed one quarte to plasma & three quarters to ISF).

The distribution of 1,000 mls of dextrose 5% is:

The ISF will increase in volume by 750 mls. The plasma volume will increase by 250 mls. This is why blood loss of 1,000 mls requires about 3 to 4 times the volume of IV replacement fluid to restore normal intravascular volume.

Plasma osmolality and tonicity will be unchanged because normal saline is isosmotic. The osmoreceptors do not contribute anything to the excretion of normal saline. Blood volume increases to 5250 mls; an increase of 5%. This is below the sensitivity of the volume receptors. It seems that the body has no clear way of excreting this excess fluid as neither osmoreceptors nor volume receptors are stimulated! However, experiments have shown that ‘replacement fluids’ are excreted the most rapidly of all these groups!

How does this happen? An additional mechanism is relevant here. Normal saline contains no protein so the oncotic pressure in the blood is slightly lowered following the saline infusion. This has 2 effects:

Plasma protein solution is a colloid and is distributed only to the intravascular fluid. The tonicity is unaltered. The blood volume increases from 5,000 mls to 6,000 mls; an increase of 20%. This is above the 7 to 10% threshold for the volume receptors. The result is a fall in ADH levels and the excretion of the excess water commences.

This water loss tends to increase the plasma oncotic pressure and water moves from the ISF to the IVF. Vascular reflexes are important also in causing venous pooling and a decrease in the ‘effective’ circulating volume. These mechanisms tend to slow the excretion of the water load. The albumin is partly slowly redistributed to the ISF and metabolised. These changes are slow so the effect of plasma protein infusion on blood volume is both more pronounced and more prolonged.

The pressure-volume control mechanisms important in long term regulation of blood volume are slow in onset but become relevant here as the blood volume change is more significant and more prolonged and occurs without change in osmolality (or initially in plasma oncotic pressure either).

Dextrose 5% is essentially treated by the body as pure water and a significant percent moves intracellularly. It is a useful fluid to replenish intracellular fluid but does so at the expense of tonicity. It is inappropriate for intravascular volume replacement. It is excreted because ADH levels decline in response to the drop in plasma osmolality.

Normal saline is a ‘replacement fluid’ (meaning ECF replacement) because it adds only to the ECF volume. Only about a third remains intravascularly. To replace intravascular volume will require transfusion with about 3 times the volume of blood lost. It is cheap and readily available. It is excreted because the small drop in plasma oncotic pressure causes glomerulotubular imbalance. ADH is not affected.