Most of the body’s water (about 65%) resides inside cells; this is called intracellular fluid (ICF).
The remaining 35%, called extracellular fluid (ECF), resides outside cells; this includes the fluid between the cells inside tissue (interstitial fluid), as well as the fluid within vessels as blood plasma and lymph.
Other extracellular fluids (cerebrospinal fluid, synovial fluid in the joints, vitreous and aqueous humors of the eye, and digestive secretions) are called transcellular fluid.
Intracellular and extracellular fluid continually mingle as fluid passes through the permeable membrane surrounding each compartment. The concentration of solutes (particularly electrolytes) within each compartment determines the amount and direction of flow.
If the concentration of electrolytes (and therefore the osmolarity) of tissue fluid increases, water moves out of the cells and into the tissues (shown in figure on left).
If the osmolarity of tissue fluid declines, water moves out of the tissues and into the cells (shown in figure on right).
The passage of fluid happens within seconds to maintain equilibrium.
Normally, the amount of water gained and lost by the body each day is equal. (An adult gains and loses about 2,500 mL fluid each day.)
Most fluid intake occurs through eating and drinking; the cells produce a fair amount of water as a by-product of metabolic reactions. (This is called metabolic water.)
Fluid is lost through the kidneys (as urine), the intestines (as feces), the skin (by sweat as well as diffusion), and the lungs (through expired air).
Water loss varies with environmental temperature and physical activity.
When total body water declines (such as by excess sweating), blood pressure drops, sodium concentration rises, and osmolarity increases. This triggers mechanisms to increase intake, as well as mechanisms to decrease output.
Mechanisms to increase intake are shown here.
The same physical changes of a decrease in blood pressure and an increase in osmolarity also trigger these changes.
In dehydration, besides a loss of fluid, the concentration of sodium (and the osmolarity) of the extracellular fluid increases. The increase in osmolarity prompts the shifting of fluid from one compartment to another in an effort to balance the concentration of sodium.
Dehydration results from consuming an inadequate amount of water to cover the amount of water lost. Other causes include diabetes mellitus and the use of diuretics. When severe, fluid deficiency can lead to circulatory collapse.
Because kidneys usually compensate, fluid excess is rarer than fluid deficit.
One cause is renal failure, in which both sodium and water are retained and the extracellular fluid (ECF) remains isotonic.
Another type is water intoxication, which can occur if someone consumes an excessive amount of water or if someone replaces heavy losses of water and sodium (such as from profuse sweating) with just water. This causes the amount of sodium in the ECF to drop; water moves into the cells, causing them to swell.
Complications of either type of fluid excess include pulmonary or cerebral edema.
Although fluid can accumulate in any organ or tissue, it typically affects the lungs, brain, and dependent areas (such as the legs).
A disturbance in any of the factors regulating the movement of fluid between blood plasma and the interstitial compartment—such as electrolyte imbalances, increased capillary pressure, and decreased concentration of plasma proteins—can trigger edema.
Electrolytes drive chemical reactions, affect distribution of the body’s water content, and determine a cell’s electrical potential.
The major cations of the body are sodium (Na+), potassium (K+), calcium (Ca+), and hydrogen (H+). The major anions are chloride (Cl−), bicarbonate (HCO3−), and phosphates (Pi).
Sodium accounts for 90% of the osmolarity of extracellular fluid.
Because it plays a key role in depolarization, it is crucial for proper nerve and muscle function.
Sodium levels are regulated by aldosterone and ADH: aldosterone adjusts the excretion of sodium, and ADH adjusts the excretion of water.
Increased renal absorption of water combined with increased water intake because of thirst cause sodium levels to decline.
Potassium is the chief cation of intracellular fluid; it works with sodium for nerve and muscle function.
Aldosterone regulates serum levels of potassium (just as it does sodium). Increasing potassium levels stimulate the adrenal cortex to secrete aldosterone, which causes the kidneys to excrete potassium as they reabsorb sodium.
Potassium imbalances are the most dangerous of any electrolyte imbalance.
Hyperkalemia may develop suddenly after a crush injury or severe burn; it may occur gradually from the use of potassium-sparing diuretics or renal insufficiency; it may cause fatal cardiac arrhythmias.
Hypokalemia often results from prolonged use of potassium-wasting diuretics. It causes muscle weakness, depressed reflexes, and cardiac arrhythmias.
Hypercalcemia leads to muscle weakness, depressed reflexes, and cardiac arrhythmia.
Hypocalcemia leads to muscle spasms and tetany.
The pH of a solution is determined by its concentration of hydrogen ions.
The body uses chemical and physiological buffers to keep acids and bases in balance.
Bicarbonate buffer system is the main buffering system; it uses bicarbonate and carbonic acid as shown in this equation: CO2 + H2O→ H2CO3→ H+ + HCO3-. The equation moves to the right when the body needs to lower pH and to the left when it needs to raise pH.
Normally, the lungs expel CO2 at the same rate metabolic processes produce it, keeping pH in balance. If CO2 begins to accumulate in the bloodstream, the respiratory physiological buffer system begins to act.
The kidneys are the only buffer system that actually expels H+ ions from the body.
Not all buffer systems act simultaneously: Chemical buffers respond first and can often restore pH within a fraction of a second. The respiratory system responds within 1 to 2 minutes. The renal system takes as long as 24 hours to be initiated.
In acidosis, plasma contains an excess concentration of H+. As the body tries to achieve acid-base balance, H+ moves out of plasma and into cells. The gain of cations inside the cell changes the polarity of the cell. To restore polarity, K+ moves out of the cell as H+ moves in. So: acidosis causes hyperkalemia.
In alkalosis, plasma contains a low concentration of H+; H+ moves out of the cells and into the plasma while K+ moves out of the plasma and into the cells. As a result: alkalosis leads to hypokalemia.
If pH is too low (metabolic acidosis), the respiratory center increases the rate of respirations. The increased respiratory rate “blows off” CO2, which raises pH. In metabolic alkalosis, the pH is too high: breathing slows, allowing CO2 to accumulate, and pH drops.
Although respiratory compensation is powerful, it does not eliminate fixed acids, such as lactic acid or ketone bodies. Renal compensation is also necessary to restore balance in those situations.
The kidneys are the most effective regulators of pH, but they take several hours to days to respond. In response to acidosis, the kidneys eliminate H+ and reabsorb more bicarbonate. In response to alkalosis, the kidneys conserve H+ and excrete more bicarbonate.