Intracellular (fluid inside the cell) = 70% of total body water and 40% of body weight

Extracelluar fluid (fluid outside the cells) - 30% of total body water and 20% of body weight

Extracellular fluid exists in 3 compartments:

1. Insterstitial (around the cells) = 75%
excess fluid in this compartment = edema

2. Intravascular (in the blood vessels) = 25%

3. Transcellular (cerebrospinal, pericardial, synovial,
intraocular, pleural, GI) **GI fluids contain electrolytes

1st spacing - fluid in its correct space
2nd spacing - edema
3rd spacing - fluid in an unusable place
- peritoneal cavity = ascites
- pericardial space = pericardial effusion

Fluid homeostasis is the dynamic interplay of three processes: fluid intake and absorption, fluid distribution, and fluid output. To maintain fluid balance, fluid intake must equal fluid output. Because some of the normal daily fluid output (e.g., urine, sweat) is a hypotonic salt solution, people must have an equivalent fluid intake of hypotonic sodium-containing fluid (or water plus foods with some salt) to maintain fluid balance (intake equal to output).

Fluid intake occurs orally through drinking but also through eating because most foods contain some water. Food metabolism creates additional water. Average fluid intake from these routes for healthy adults is about 2300 mL, although this amount can vary widely depending on exercise habits, preferences, and the environment. Other routes of fluid intake include intravenous (IV), rectal (e.g., enemas), and irrigation of body cavities that can absorb fluid.

Sensible losses = measurable; urine and feces

Insensensible losses = not able to be measured; skin and lungs

Many different processes are involved in the movement of electrolytes and water between the ICF and ECF.
Diffusion is the movement of molecules across a permeable membrane from an area of high concentration to one of low concentration (see next slide).
The net movement of molecules stops when the concentrations are equal on both sides of semipermeable membrane.
Simple diffusion is passive and requires no external energy.
Facilitated diffusion involves the use of a protein carrier in the cell membrane to move molecules that cannot otherwise pass through the membrane. Glucose transport into the cell is an example of facilitated diffusion. A carrier molecule on most cells increases or facilitates the rate of diffusion of glucose into these cells.

Osmosis is the movement of water through a semipermeable membrane that does not allow solutes to cross.
Water moves from the less concentrated side (has more water) to the more concentrated side (has less water).
Requires no energy.
Osmolality is nearly the same in the various body fluid spaces. Therefore measuring or estimating plasma osmolality is a useful way to assess the state of the body's water balance.
Normal plasma osmolality is between 280 and 295 mOsm/kg.
Osmolarity measures the total milliosmoles per liter of solution, or the concentration of molecules per volume of solution (mOsm/L).
Osmolality measures the number of milliosmoles per kilogram of water, or the concentration of molecules per weight of water. Osmolality is the preferred measure to evaluate the concentration of plasma, urine, and body fluids.


Active transport uses external energy to move molecules against the concentration gradient—from an area of low concentration to an area of high concentration.
An example of active transport is the sodium-potassium pump. ATP is used to move sodium out of the cell and potassium into the cell.

Capillary hydrostatic pressure and interstitial oncotic pressure move water out of the capillaries. Plasma oncotic pressure and interstitial hydrostatic pressure move fluid into the capillaries.
If capillary or interstitial pressures change, fluid may shift abnormally from one compartment to another, resulting in either edema or dehydration.
Hydrostatic pressure is the force of fluid in a compartment pushing against a cell membrane or vessel wall.

In the blood vessels, hydrostatic pressure is the BP generated by the contraction of the heart. At the capillary level, hydrostatic pressure is the major force that pushes water out of the vascular system and into the interstitial space.
Oncotic pressure (colloidal osmotic pressure) is the osmotic pressure caused by plasma colloids in solution. The plasma protein molecules attract water, pulling fluid from the tissue space to the vascular space.

Edema, an accumulation of fluid in the interstitial space, occurs if venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic pressure rises. Edema may also develop if an obstruction of lymphatic outflow causes decreased removal of interstitial fluid.
An increase in the plasma osmotic or oncotic pressure draws fluid into the plasma from the interstitial space. This can occur with administration of colloids, dextran, mannitol, or hypertonic solutions. Additionally, an increase in tissue hydrostatic pressure can cause a shift of fluid into the plasma. Wearing elastic compression gradient stockings to decrease peripheral edema is a therapeutic application of this effect.

Elderly - decreased kidney function, loss of subcutaneous tissue, moisture loss, decreased thirst mechanism

Infants/Children - increased fluid output r/t size, more rapid disturbances, slower adjustment

Comatose/bedridden/confused patients - decreased intake ability, illness, therapeutic meausures

Thirst, the conscious desire for water, is an important regulator of fluid intake when plasma osmolality increases (osmoreceptor-mediated thirst) or the blood volume decreases (baroreceptor-mediated thirst and angiotensin II– and III–mediated thirst). The thirst-control mechanism is located within the hypothalamus in the brain. Osmoreceptors continually monitor plasma osmolality; when it increases, they cause thirst by stimulating neurons in the hypothalamus.

Fluid output normally occurs through four organs: the skin, lungs, GI tract, and kidneys.
The GI tract plays a vital role in fluid balance. Approximately 3 to 6 L of fluid moves into the GI tract daily and then returns again to the ECF. The average adult normally excretes only 100 mL of fluid each day through feces. However, diarrhea causes a large fluid output from the GI tract.
The kidneys are the major regulator of fluid output because they respond to hormones that influence urine production. When healthy adults drink more water, they increase urine production to maintain fluid balance. If they drink less water, sweat a lot, or lose fluid by vomiting, their urine volume decreases to maintain fluid balance. These adjustments primarily are caused by the actions of antidiuretic hormone (ADH), the renin-angiotensin-aldosterone system (RAAS), and atrial natriuretic peptides (ANPs).
ADH regulates the osmolality of the body fluids by influencing how much water is excreted in urine. It is synthesized by neurons in the hypothalamus that release it from the posterior pituitary gland. ADH circulates in the blood to the kidneys, where it acts on the collecting ducts.
People normally have some ADH release to maintain fluid balance. More ADH is released if body fluids become more concentrated. Factors that increase ADH levels include severely decreased blood volume (e.g., dehydration, hemorrhage), pain, stressors, and some medications.
The RAAS regulates ECF volume by influencing how much sodium and water are excreted in urine. It also contributes to regulation of blood pressure.
Aldosterone circulates to the kidneys, where it causes resorption of sodium and water in isotonic proportion in the distal renal tubules. Removing sodium and water from the renal tubules and returning it to the blood increases the volume of the ECF.
To maintain fluid balance, normally some action of the RAAS occurs.
ANP also regulates ECV by influencing how much sodium and water are excreted in urine. Cells in the atria of the heart release ANP when they are stretched (e.g., by an increased ECV). ANP is a weak hormone that inhibits ADH by increasing the loss of sodium and water in the urine (see Fig. 42-6, C). Thus ANP opposes the effect of aldosterone.

Edema, an accumulation of fluid in the interstitial space, occurs if venous hydrostatic pressure rises, plasma oncotic pressure decreases, or interstitial oncotic pressure rises. Edema may also develop if an obstruction of lymphatic outflow causes decreased removal of interstitial fluid.
An increase in the plasma osmotic or oncotic pressure draws fluid into the plasma from the interstitial space. This can occur with administration of colloids, dextran, mannitol, or hypertonic solutions. Additionally, an increase in tissue hydrostatic pressure can cause a shift of fluid into the plasma. Wearing elastic compression gradient stockings to decrease peripheral edema is a therapeutic application of this effect.

Fluid spacing: the distribution of body water
First spacing: the normal distribution of fluid in the ICF and ECF compartments
Second spacing: an abnormal accumulation of interstitial fluid (i.e., edema)
Third spacing: when excess fluid collects in the nonfunctional area between cells. This fluid is trapped where it is difficult or impossible for it to move back into the cells or blood vessels. Third-spaced fluid is trapped and unavailable for functional use. Ascites is an example of third-spaced fluid.

One liter of water weighs 2.2 lb (1 kg)
Body weight change is an excellent indicator of overall fluid volume loss or gain
5% loss = clinically signficant
15% loss = fatal
Measuring Daily Weights
-Same scale
-Same time
-Same amount of clothing
I&O, Labs

If disease processes, medications, or other factors disrupt fluid intake or output, imbalances sometimes occur. For example, with diarrhea, fluid output is increased, and a fluid imbalance (dehydration) occurs if fluid intake does not increase appropriately.
Two major types of fluid imbalances are known: volume imbalances and osmolality imbalances.
Volume imbalances are disturbances of the amount of fluid in the extracellular compartment.
Osmolality imbalances are disturbances of the concentration of body fluids.
Volume and osmolality imbalances may occur separately or in combination.

Fluid volume excess may result from excess intake of fluids, abnormal retention of fluids (e.g., heart failure, renal failure), or a shift of fluid from interstitial fluid into plasma fluid, increasing intravascular volume.

ECV excess occurs when too much isotonic fluid is found in the extracellular compartment. Intake of sodium-containing isotonic fluid has exceeded fluid output. For example, when you eat more salty foods than usual and drink water, you may notice that your ankles swell or rings on your fingers feel tight, and you gain 2 lbs (1 kg) or more overnight. These are manifestations of mild ECV excess.

Hyponatremia, also called water excess or water intoxication, is a hypotonic condition. It arises from gain of relatively more water than salt or loss of relatively more salt than water. The excessively dilute condition of interstitial fluid causes water to enter cells by osmosis, causing the cells to swell. Signs and symptoms of cerebral dysfunction occur when brain cells swell.

Fluid volume deficit can occur from loss of body fluids (e.g., diarrhea, vomiting, hemorrhage, polyuria), inadequate fluid intake, or a plasma to interstitial fluid shift.

ECV deficit is present when isotonic fluid is insufficient in the extracellular compartment. Remember that a lot of sodium is found in normal ECF. With ECV deficit, output of isotonic fluid exceeds intake of sodium-containing fluid. Because ECF is both vascular and interstitial, signs and symptoms arise from lack of volume in both of these compartments.

In an osmolality imbalance, body fluids become hypertonic or hypotonic, and this causes osmotic shifts of water across cell membranes. Osmolality imbalances are called hypernatremia and hyponatremia.

Hypernatremia, also called water deficit (hypertonic dehydration), is a hypertonic condition. One of two general causes make body fluids too concentrated: loss of relatively more water than salt, or gain of relatively more salt than water. When the interstitial fluid becomes hypertonic, water leaves cells by osmosis, and they shrivel. Signs and symptoms of hypernatremia are those of cerebral dysfunction, which arise when brain cells shrivel.
Causes: Inadequate water intake, concentrated feedings, DI

ECV deficit and hypernatremia often occur at the same time; this combination is called clinical dehydration. The ECV is too low, and the body fluids are too concentrated. Clinical dehydration is common with gastroenteritis or other causes of severe vomiting and diarrhea when people are not able to replace their fluid output with enough intake of dilute sodium-containing fluids. Signs and symptoms of clinical dehydration are those of both ECV deficit and hypernatremia.

The goal of IV fluid administration is to correct or prevent fluid and electrolyte disturbances. IVs allow direct access to the vascular system, permitting continuous infusion of fluids over a period of time.


An IV solution may be isotonic, hypotonic, or hypertonic.
Isotonic solutions have the same effective osmolality as body fluids. Sodium-containing isotonic solutions, such as normal saline, are indicated for ECV replacement to prevent or treat ECV deficit. EX. NS, LR, D5W, D51/2NS

Hypotonic solutions have an effective osmolality less than body fluids, thus decreasing osmolality by diluting body fluids and moving water into cells. EX. 0.33% NS D1/4W

Hypertonic solutions have an effective osmolality greater than body fluids. If they are hypertonic sodium-containing solutions, they increase osmolality rapidly and pull water out of cells, causing them to shrivel. EX. D10W, 3%NS, TPN, Albumin

Additives such as potassium chloride (KCl) are common in IV solutions. A health care provider’s order is necessary if an IV is to have additives added.

An easy visual to understand the impact of tonicity on fluid movement is to picture what may happen to red blood cells when you administer different IV fluids.
Isotonic fluids have no impact on the red bloods cells.
If a cell is surrounded by hypotonic fluid, water moves into the cell, causing it to swell and possibly to burst.
If a cell is surrounded by hypertonic fluid, water leaves the cell to dilute the ECF; the cell shrinks and eventually may die.

Electrolyte composition varies between the ICF and ECF.
The most prevelant cation in ICF is potassium, with small amounts of magnesium and sodium. The main anion is phosphate, with some protein and a small amount of bicarbonate.
The main cation in ECF is sodium, with small amounts of potassium, calcium, and magnesium. The main anion is chloride with small amounts of bicarbonate, sulfate, and phosphate.

Sodium is the primary determinant of ECF osmolality.
The serum sodium level reflects the ratio of sodium to water, not necessarily the amount of sodium in the body. Changes in the serum sodium level can reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two.
Sodium imbalances are typically associated with ECF imbalances

Sodium plays a role in the generation and transmission of nerve impulses, muscle contractility and acid-base balance.

The GI tract absorbs sodium from foods. Typically, daily intake of sodium far exceeds the body's daily requirements.
Sodium leaves the body through urine, sweat, and feces. The kidneys are the primary regulator of sodium balance.

Symptomatic hypernatremia is rare.
When symptoms do occur, they are primarily the result of water shifting out of cells into the ECT with resultant dehydration and shrinkage of cells.
Dehydration of brain cells results in alterations in mental status, ranging from agitation, restlessness, confusion, and lethargy to coma.
If there is an accompanying ECF volume deficit, manifestations such as postural hypotension, tachycardia, and weakness occur.

Hyponatremia may result from a loss of sodium-containing fluids, water excess in relation to the amount of sodium (dilutional hyponatremia), or a combination of both.
Common causes of hyponatremia from loss of sodium-rich body fluids include profuse diaphoresis, draining wounds, excessive diarrhea or vomiting, and and primary adrenal insufficiency.
Inappropriate use of sodium-free or hypotonic IV fluids causes hyponatremia from water excess. This may occur in patients after surgery or major trauma or administering of fluids in patients with renal failure. Patients with psychiatric disorders may have an excessive water intake. SIADH will result in dilutional hyponatremia caused by abnormal retention of water.
Clinical manifestations are the result of cellular swelling and are first manifested in the CNS.

Potassium is the major ICF cation, with 98% of the body potassium being intracellular. For example, potassium concentration within muscle cells is around 140 mEq/L; potassium concentration in the ECF is 3.5 to 5.0 mEq/L.
The sodium-potassium pump in cell membranes maintains this concentration difference by pumping potassium into the cell and sodium out. Insulin helps by stimulating the sodium-potassium pump.
Because the ratio of ECF to ICF potassium is the major factor in the resting membrane potential of nerve and muscle cells, neuromuscular and cardiac function are often affected by potassium imbalances.
Potassium is involved with regulating intracellular osmolality and promoting cellular growth.
Potassium is required for glycogen to be deposited in muscle and liver cells.
Potassium also plays a role in acid-base balance.

Diet is the source of potassium. The typical Western diet contains approximately 50 to 100 mEq of potassium daily, mainly from fruits, dried fruits, and vegetables.
Many salt substitutes used in low-sodium diets contain substantial potassium.
Patients may receive potassium from parenteral sources, including IV fluids; transfusions of stored, hemolyzed blood; and medications (e.g., potassium penicillin).
The kidneys are the primary route for potassium loss, eliminating about 90% of the daily potassium intake. Potassium excretion depends on the serum potassium level, urine output, and renal function. When serum potassium is high, urine potassium excretion increases and when serum levels are low, excretion decreases. Large urine output can cause excess potassium loss. Impaired kidney function can cause potassium retention. There is an inverse relationship between sodium and potassium reabsorption in the kidneys.

Hypokalemia is abnormally low potassium concentration in the blood. Hypokalemia results from decreased potassium intake and absorption, a shift of potassium from the ECF into cells, and an increased potassium output. Common causes of hypokalemia from increased potassium output include diarrhea, repeated vomiting, and use of potassium-wasting diuretics. People who have these conditions need to increase their potassium intake to reduce their risk of hypokalemia. Hypokalemia causes muscle weakness, which becomes life threatening if it includes respiratory muscles and potentially life-threatening cardiac dysrhythmias.

Hyperkalemia is abnormally high potassium ion concentration in the blood. Its general causes are increased potassium intake and absorption, shift of potassium from cells into the ECF, and decreased potassium output. People who have oliguria (decreased urine output) are at high risk of hyperkalemia from the resultant decreased potassium output unless their potassium intake also decreases substantially. Understanding this principle helps you remember to check urine output before you administer IV solutions containing potassium. Hyperkalemia can cause muscle weakness, potentially life-threatening cardiac dysrhythmias, and cardiac arrest.

Hypermagnesemia usually occurs only with an increase in magnesium intake accompanied by renal insufficiency or failure.
A patient with chronic kidney disease who ingests products containing magnesium (e.g., Maalox, milk of magnesia) will have a problem with excess magnesium.
Magnesium excess could develop in the pregnant woman who receives magnesium sulfate for the management of eclampsia.

Hypocalcemia is abnormally low calcium concentration in the blood. The physiologically active form of calcium in the blood is ionized calcium. Total blood calcium also contains inactive forms that are bound to plasma proteins and small anions such as citrate. Factors that cause too much ionized calcium to shift to bound forms cause symptomatic ionized hypocalcemia. People who have acute pancreatitis frequently develop hypocalcemia because calcium binds to undigested fat in their feces and is excreted. This process decreases absorption of dietary calcium and increases calcium output by preventing resorption of calcium contained in GI fluids. Hypocalcemia increases neuromuscular excitability, which is the basis for its signs and symptoms.

Hypercalcemia is abnormally high calcium concentration in the blood. Hypercalcemia results from increased calcium intake and absorption, shift of calcium from bones into the ECF, and decreased calcium output. Patients with cancer often develop hypercalcemia because some cancer cells secrete chemicals into the blood that are related to parathyroid hormone. When these chemicals reach the bones, they cause shift of calcium from bones into the ECF. This weakens bones, and the person sometimes develops pathological fractures (i.e., bone breakage caused by forces that would not break a healthy bone). Hypercalcemia decreases neuromuscular excitability, the basis for its other signs and symptoms, the most common of which is lethargy.

Hypermagnesemia usually occurs only with an increase in magnesium intake accompanied by renal insufficiency or failure.
A patient with chronic kidney disease who ingests products containing magnesium (e.g., Maalox, milk of magnesia) will have a problem with excess magnesium.
Magnesium excess could develop in the pregnant woman who receives magnesium sulfate for the management of eclampsia.
Excess magnesium inhibits acetylcholine release at the myoneural junction and calcium movement into cells, impairing nerve and muscle function.
Initial manifestations include hypotension, facial flushing, lethargy, urinary retention, nausea, and vomiting.
As the serum magnesium level increases, deep tendon reflexes are lost, followed muscle paralysis and coma.
Respiratory and cardiac arrest can occur.



Hypomagnesemia occurs in patients with limited magnesium intake or increased renal losses.
Major causes of hypomagnesemia from insufficient food intake include prolonged fasting or starvation and chronic alcoholism.
Fluid loss from the GI tract interferes with magnesium absorption.
Another potential cause of hypomagnesemia is prolonged parenteral nutrition without magnesium supplementation.
Many diuretics increase the risk of magnesium loss through renal excretion.
In addition, osmotic diuresis caused by high glucose levels in uncontrolled diabetes mellitus increases renal excretion of magnesium.
Clinically, hypomagnesemia resembles hypocalcemia. Neuromuscular manifestations are common, such as muscle cramps, tremors, hyperactive deep tendon reflexes, Chvostek’s sign and Trousseau’s sign. Neurologic manifestations include confusion, vertigo, and seizures.
Magnesium deficiency can lead to cardiac dysrhythmias, such as torsade de pointes and ventricular fibrillation.

Phosphorus is the primary anion in the ICF and the second most abundant element in the body after calcium. Most phosphorus is in the bones and teeth as calcium phosphate.
The remaining phosphorus is metabolically active and essential to the function of muscle, RBCs, and the nervous system.
It is also involved in the acid-base buffering system, the mitochondrial formation of ATP, cellular uptake and use of glucose, and the carbohydrate, protein, and fat metabolism.

PTH maintains serum phosphorus levels and balance.
Proper phosphate balance requires adequate renal functioning because the kidneys are the major route of phosphate excretion. When the phosphate level in the glomerular filtrate falls below the normal level or PTH levels are low, the kidneys reabsorb additional phosphorus.
A reciprocal relationship exists between phosphorus and calcium in that a high serum phosphate level tends to cause a low calcium concentration in the serum. This means a low serum calcium levels stimulate the release of PTH, decreasing reabsorption of phosphorus and lowering phosphorus levels

Hyperphosphatemia is commonly caused by acute kidney injury or chronic kidney disease, which alter the kidney’s ability to excrete phosphate.
Other causes include excess phosphate intake from the use of phosphate-containing laxatives or enemas or a shift of phosphate from ICF to ECF. This may occur in patients with tumor lysis syndrome or rhabdomyolysis.
Hypoparathyroidism and vitamin D intoxication cause increased kidney phosphate reabsorption.
Hyperphosphatemia is often asymptomatic unless calcium binds with phosphate, leading to manifestations of hypocalcemia.
These manifestations include tetany, muscle cramps, paresthesias, and seizures. Long term, increased phosphate levels result in the development of calcified deposits outside of the bones.
These calcium deposits can be found in soft tissues such as joints, arteries, skin, corneas, and kidneys and produce organ dysfunction, notably renal failure.


Hypophosphatemia (low serum phosphate) can result from decreased intestinal absorption, increased urinary excretion, or from ECF to ICF shifts. Malabsorption, diarrhea, and phosphate-binding antacids lead to decreased absorption.
Hypophosphatemia may also occur in those who are malnourished or receive parenteral nutrition with inadequate phosphorus replacement.
Most of the manifestations of hypophosphatemia result from impaired cellular energy and oxygen delivery related to deficient cellular ATP and 2,3-diphosphoglycerate (2,3-DPG), an enzyme in RBCs that facilitates oxygen delivery to the tissues.
Mild to moderate hypophosphatemia is often asymptomatic.
Severe hypophosphatemia may be fatal because of decreased cellular function.
Acute manifestations include CNS depression, muscle weakness and pain, respiratory failure, and heart failure. Chronic hypophosphatemia alters bone metabolism, resulting in rickets and osteomalacia.
Managing mild phosphorus deficiency involves increasing oral intake with dairy products or phosphate supplements. Dairy products are better tolerated as phosphate supplements are often associated with adverse GI effects.
Symptomatic hypophosphatemia can be fatal and often requires IV administration of sodium phosphate or potassium phosphate.
Frequent monitoring of serum phosphate and calcium levels is necessary to guide IV therapy. Sudden symptomatic hypocalcemia, secondary to increased calcium phosphorus binding, is a potential complication of IV phosphorus administration.

Normal acid-base balance is maintained with acid excretion equal to acid production. Acids release hydrogen (H+) ions; bases (alkaline substances) take up H+ ions. The more H+ ions that are present, the more acidic is the solution.
If the pH goes outside the normal range, enzymes within cells do not function properly; hemoglobin does not manage oxygen properly; and serious physiological problems occur, including death. Laboratory tests of a sample of arterial blood called arterial blood gases (ABGs) are used to monitor a patient’s acid-base balance.

Production: Cellular metabolism constantly creates two types of acids: carbonic acid and metabolic acids. Cells produce carbon dioxide (CO2), which acts as an acid in the body by converting to carbonic acid.
Metabolic acids are any acids that are not carbonic acid. They include citric acid, lactic acid, and many others.

Buffering: If too many free H+ ions are present, a buffer takes them up, so they no longer are free. If too few are present, a buffer can release H+ ions to prevent an acid-base imbalance. Buffers work rapidly—within seconds.
All body fluids contain buffers. The major buffer in ECF is the bicarbonate (HCO3−) buffer system, which buffers metabolic acids. It consists of a lot of bicarbonate and a small amount of carbonic acid (normally a 20:1 ratio). Addition of H+ released by a metabolic acid to a bicarbonate ion makes more carbonic acid. Now the H+ is no longer free and will not decrease the blood pH.
If too few H+ ions are present, the carbonic acid portion of the buffer pair will release some, increasing the bicarbonate, again returning pH to normal.
Other buffers include hemoglobin, protein buffers, and phosphate buffers. Cellular and bone buffers also contribute. Buffers normally keep the blood from becoming too acid when acids that are produced by cells circulate to the lungs and kidneys for excretion.

The body has two acid excretion systems: lungs and kidneys. The lungs excrete carbonic acid; the kidneys excrete metabolic acids.
When you exhale, you excrete carbonic acid in the form of CO2 and water. If the PaCO2 (i.e., level of CO2 in the blood) rises, the chemoreceptors trigger faster and deeper respirations to excrete the excess. If the PaCO2 falls, the chemoreceptors trigger slower and shallower respirations, so more of the CO2 produced by cells remains in the blood and makes up the deficit. These alterations in respiratory rate and depth maintain the carbonic acid portion of acid-base balance. Sometimes people who have lung disease have difficulty with normal excretion of carbonic acid, which causes it to accumulate and make the blood more acid.
The kidneys excrete all acids except carbonic acid. They secrete H+ into the renal tubular fluid, putting HCO3− back into the blood at the same time. If too many H+ ions are present in the blood, renal cells move more H+ ions into the renal tubules for excretion, retaining more HCO3− in the process. If too few H+ ions are present in the blood, renal cells secrete fewer H+ ions. Phosphate buffers in the renal tubular fluid keep the urine from becoming too acidic when the kidneys excrete H+ ions. If the kidneys need to excrete a lot of H+, renal tubular cells secrete ammonia, which combines with H+ ions in the tubules to make NH4+, ammonium ions. Buffering by phosphate and the creation of NH4+ turn free H+ ions into other molecules in the renal tubular fluid. This process enables metabolic acid excretion in urine without making urine too acidic. People who have kidney disease often have difficulty with normal excretion of metabolic acids.

Used to correct mild fluid and electrolyte deficits
Glucose not only provides calories, but also promotes sodium and water absorption in the small intestine.
Commercial oral rehydration solutions are now available for home use.
Cola drinks are avoided because they do not contain adequate electrolyte replacement and the sugar content may lead to osmotic diuresis.