Oncotic pressure, osmolality, and tonicity (Proceedings)
The underpinnings of your fluid therapy choices
Apr 01, 2008
CVC IN WASHINGTON, D.C. PROCEEDINGS
Osmotic "control" of transmembrane fluid flux
Oncotic PressureColloids are large molecules that are not freely permeable across the vascular membrane, are present in the vascular fluid compartment in larger concentrations than in the interstitium, and therefore are osmotically responsible for retaining crystalloids within the vascular fluid compartment according to the Starling equilibrium of transvascular fluid flux, assuming normal vascular permeability.
Albumin is the prominent intravascular colloid. Hypoproteinemia may be associated with simultaneous hypovolemia, and subcutaneous edema and ascites. This is not a straight-line relationship since decreases in plasma albumin concentration are initially offset by a dilutional decrease in perivascular albumin concentration. An increased capillary permeability to the extent that albumin and other colloids are freely permeable would also result in hypovolemia and interstitial edema. Crystalloids are freely permeable across the vascular membrane. Changes in sodium concentration have no effect on transvascular fluid flux. Intravenously administered crystalloid fluids are rapidly redistributed to the interstitial fluid compartment in an amount proportional to the relative size of the interstitial fluid compartment.
Normal colloid osmotic pressure is 20 to 25 mm Hg. Values in the high "teens" are common in critically ill patients but are not considered to warrant treatment, per se. Values in the low "teens" are considered to be too low, and warrant treatment with an artificial colloid or plasma. Values in the single digits (commonly seen in patients with portocaval shunts) also need to be treated but there is a need to do it slowly. Rapid administration of colloids to these patients has caused edema, presumably by increasing capillary hydrostatic pressure ahead of increases in colloid osmotic pressure and upsetting the precariously balanced starling forces.
Sodium is pumped out of the cell by the sodium-potassium-ATPase pump in the cellular membrane. As sodium and its related anion (predominantly chloride and bicarbonate) are maintained in the extravascular fluid compartment, they are primarily responsible for the osmotic attraction and retention of water in the extracellular fluid compartment.
Acute changes in extracellular sodium concentration result in transcellular fluid fluxes (hyponatremia causes cellular edema; hypernatremia causes cellular dehydration). Diseases associated with inadequate cellular energy production and ATP depletion are associated with the influx of sodium (and water) into the cell, cellular edema, and, eventually, cellular disruption. The endothelial membrane is freely permeable to these crystalloids and sodium concentration has no impact upon the transvascular fluid flux.
It is actually extracellular osmolality, rather than sodium concentration, that is important to transcellular fluid flux. Sodium (and its related anion) are by far the largest component of measured osmolality. Osmolality is normally calculated as 2 x [Na+] + 10 (which accounts for the normal contributions of glucose and blood urea nitrogen [BUN]). If the glucose and BUN are known, their contributions can be calculated as glucose (mg/dl)/18 + BUN (mg/dl)/2.8. While hyponatremia is the only cause of hypo-osmolality, there are many causes of hyperosmolality. The measured osmolality is normally about 10 to 15 mOsm/Kg higher than the calculated value. A higher osmolar gap is indicative of unmeasured osmols.