While the importance of water and electrolytes has been highlighted, health professionals were observed to have poor knowledge and practice of fluid and electrolyte therapy.
The intravascular (IVS) and extravascular (ISS) components of the ECF are separated by the capillary membrane, which allow only a slow escape rate of albumin (5%/hr)
1. Fluids and electrolytes flow between the ECF and the GI tract involving active secretion and reabsorption of digestive juices
2. The relationship between them constitute the internal fluid balance
3. The external fluid and electrolyte balance between the body and its environment is defined by the intake of fluid and electrolytes versus the output from the kidneys, the gastrointestinal tract, and the skin and lungs
Since external and internal balances could be disturbed by disease, it is important to understand normal physiology and explain the disorders happening in patients.
Our intake should match the needs of bodily functions, maintaining a zero balance in which intake and output are equal and physiological osmolality (280-290mOsm/kg is maintained.
Evaporation of water from the lungs and skin occurs all the time. The average in temperate climate is 0.5 to 1 liter/day but in a warm environment, during fever, or with exertion, additional sweat containing up to 50mmol/L of salt.
The intestine absorbs water and electrolytes very efficiently so that fluid loss is only about 100-150mL/day; in the presence of disease, this may be greatly increased.
Main organ for regulating fluid and electrolyte balance and also excreting waste products of metabolism. Its activity is controlled by pressure and osmotic sensors and secretion of hormones.
1. Organs, which sense the changes in osmolality of plasma (osmoreceptors), are located in the hypothalamus and signal the posterior pituitary gland to increase or decrease its secretion of vasopressin or antidiuretic hormone (ADH)
2. Dilution of the ECF, including plasma, by intake of water or fluid of osmolality lower than plasma, causes ADH secretion to fall, so that the distal tubules of the renal glomeruli excrete more water and produce a dilute urine
3. Conversely, dehydration causes the ECF to become more concentrated, ADH secretion rises and the renal tubules reabsorb more water, producing a concentrated urine
4. In response to dehydration, the normal kidney can concentrate urea in the urine up to a hundred-fold, so that the normal daily production of urea during protein metabolism can be excreted in as little as 500 ml of urine
5. Age and disease can impair renal concentrating capacity, large volume of urine needed to excrete same amount of waste products
6. High protein intake or increased catabolism = a large volume of urine is needed to clear urea
7. Measurement of both urinary volume and concentration (osmolality) are important (serum urea, creatinine concentration)
1. Pressure sensors in the circulation are stimulated and these excite renin secretion by the kidney
2. Renin stimulates aldosterone secretion by the adrenal gland
3. Aldosterone acts on the renal tubules, causing them to reabsorb and conserve Na+
4. The mechanism for maintaining sodium balance may be disturbed in disease, leading to Na+ deficiency or commonly to excess sodium retention with consequent edeme and adverse clinical outcome
Its concentration has to be maintained within narrow limits (3.5-5.3 mmol/L) to avoid the risk of muscular dysfunction or potentially fatal cardiac events
This is achieved by exchange of K+ in the renal tubules for Na+ and H+, allowing more or less K+ to be excreted
In the presence of K+ deficiency, H+ ion reabsorption is impaired leading to hypokalemic alkalosis
Diseases like gastroenteritis, diabetic ketoacidosis or Addison's disease cause their own specific changes in fluid and electrolyte balance, but there are non-specific changes which occur in response to any form of injury or inflammation, which have important implications for management, particularly of surgical patients.
The response to injury, stress and sepsis results in an increase in the size of the pores in the capillary membrane and the transcapillary escape rate of albumin increases from about 5%/h in health to 13-15%/h. This phenomenon can last from several hours to days.
Albumin leaks out from the IVS into the ISS and along with it, water and sodium are drawn into the ISS. This results in the contraction of the IVS, and the expansion of the IVS.
As the return of albumin into the circulation via lymphatics is unchanged, the net result is intravascular hypovolemia with edema.
K+ losses after surgery, sepsis or trauma are not only secondary to increased secretion, but also to protein and glycogen catabolism.
In situations where catabolism is extreme and renal function is impaired, the outflow of K+ from the cells may exceed the kidney's capacity to excrete it, causing hyperkalemia.
In the convalescent phase, as net intracellular protein and glycogen anabolism is restored, the cells take up K+ again and the patient's potassium intake has to be increased or else hypokalemia will develop.
That part of the TBW contained within the cells, approximately 40% of body weight and 2/3rds of TBW. Muscle cells contain 75% water and fat cells have <5% water
That part of the ECF contained within the circulation and supported oncotically by the plasma proteins, separated from the interstitial fluid by the capillary membrane. Comprises approximately 3-4% of the body weight