The amount of water a patient requires each day depends on the patient’s age and the nature of the patient’s medical condition. Water is 30 mL/kg of body weight.
A patient who weighs 70 kg has 2100 mL of water (70 kg x 30 mL/kg). In other words, a patient who weighs 150 lbs weighs 68 kg (150 lbs/2.2 lbs/kg) and has 2240 mL of water.
Each day the patient losses:
This means that each day the patient must take in between 1900 mL and 2400 mL of fluid in order to maintain fluid-electrolyte balance. However, disease and the treatment of disease can increase the patient’s output of water requiring that the patient increase the intake of water.
For example, a patient who has a fever loses as much as 15% more water than the normal daily water loss. That is, the patient loses between 2185 mL and 2760 mL of water each day when he or she has a fever.
FLUID REPLACEMENT AND THE NURSING PROCESS
When a patient is experiencing the loss of fluid, the nurse should:
Potential nursing diagnoses for a patient that is receiving fluid volume replacement therapy are:
Before beginning fluid replacement therapy, goals should include:
When fluid replacement therapy is underway, make sure to monitor:
The patient should be taught:
The nurse must frequently evaluate the patient’s
Potassium is an electrolyte cation that is more prevalent inside cells than it is in extra cellular fluid. It is used to transmit and conduct neurological impulses and to maintain cardiac rhythms. Potassium is also used to contract skeletal and smooth muscles.
In order for a muscle to contract, the concentration of potassium inside the cell moves out and is replaced by sodium, which is the prevalent electrolyte outside the cell (see Sodium). These electrolytes reverse position when the muscle re polarizes. The concentration of potassium and sodium is maintained by the sodium-potassium pump found in cell membranes. The sodium-potassium pump uses adenosine triphosphate (ATP) to pump potassium back into the cell and sodium out of the cell.
Potassium regulates intracellular osmolality and promotes cell growth. It moves into cells as new tissues form and leaves cells when tissues break down. Patients receive potassium from their diet and excrete potassium in urine (90%) and feces (8%).
Serum potassium is measured to determine if the patient has a normal range of potassium. The normal serum potassium is between 3.5 to 5.3 milliequiva-lents per liter (mEq/L). Caution: Serum potassium less than 2.5 mEq/L or greater than 7.0 mEq/L can cause the patient to have a cardiac arrest. Diseases such as kidney disease can cause potassium to become imbalanced. When this happens, the patient will exhibit specific signs and symptoms and the serum potassium will be outside the normal range.
Hyperkalemia occurs when a patient has a serum potassium level greater than 5.3 mEq/L. A number of factors can cause this condition including:
The nurse should monitor a patient for the signs and symptoms of hyperkalemia. The more common of these are:
The nurse must respond quickly once signs and symptoms of hyperkalemia develop as the patient is at risk for seizures, injury related to muscle weakness, and cardiac arrhythmias. Here is what needs to be done.
Hypokalemia occurs when a patient has a serum potassium level of less than 3.5 mEq/L. A number of factors can cause this condition. These include:
The patient may have the following signs and symptoms when experiencing hypokalemia:
The patient may also exhibit an abnormal EKG that shows:
The nurse must respond with the following interventions as the patient is a risk for injury related to muscle weakness and cardiac arrhythmias.
Caution: This deficit cannot be corrected rapidly. The infusion should not exceed 10 to 20 mEq per hour or the patient may experience hyperkalemia and can experience cardiac arrest. Be alert that infusions containing potassium may cause pain at the IV insertion site. If urine output is 30 mL/hour notify prescriber. Infusions should not contain more than 60 mEq/L of potassium chloride (KCl). 40 mEq/L is the preferred amount to add to 1000 mL of intravenous solution.
Warning: NEVER give potassium as an intravenous push or intravenous bolus. This will cause immediate cardiac arrest which is not reversible with Potassium supplements.
cardiopulmonary resuscitation. Potassium must be diluted in IV fluids as stated above. Don’t give potassium if the patient suffers from renal insufficiency, renal failure, or Addison’s disease. Do not give potassium if the patient has hyper-kalemia, severe dehydration, acidosis, or takes potassium-sparing diuretics. Use with caution with patients who have cardiac disorders or burns.
Sodium is the major cation in extracellular fluid found in tissue spaces and ves-sels. Sodium plays an important role in the regeneration and transmission of nerve impulses and affects water distribution inside and outside cells. It is part of the sodium/potassium pump that causes cellular activity. When it shifts into the cell, depolarization (contraction) occurs; when it shifts out of the cell, potassium goes back into the cell and repolarization (relaxation) occurs. Sodium also combines readily in the body with chloride (Cl) or bicarbonate (HCO3) to pro-mote acid-base balance (pH).
The patient receives sodium when food is absorbed in the GI tract. Typically, a patient takes in more sodium than the patient’s daily requirement. The kidneys regulate the sodium balance by retaining urine when the sodium concentration is low and excreting urine when the sodium concentration is high. Most excess sodium is excreted in urine although sodium also leaves the patient as perspira-tion and in feces.
The serum sodium level, which is the ratio of sodium to water, is the indicator of the sodium level in a patient’s body. Sodium is measured in milliequivalents per liter (mEq/L). The normal range of serum sodium is from 135 mEq/L to 145 mEq/L.
A patient’s serum sodium level moves out of the normal range when the patient is retaining too much or too little water, has a high or low concentrations of sodium, or a combination of both. A patient is hypernatremic when there is a high concentration of sodium and hyponatremic when there is a low concentration of sodium.
Hypernatremia occurs when the patient’s serum sodium is greater than 145 mEq/L.This happens for one of two reasons: The patient’s sodium concentration has increased while the volume of water remains unchanged or the patient’s water volume has decreased while the sodium concentration remains unchanged.
Regardless of what happened, the patient experiences hyperosmolality, which is a higher-than-normal concentration of sodium. This causes water to shift out of cells and into extra cellular space resulting in cellular dehydration. A patient who is alert and can drink water to quench a thirst is at less risk for hypernatremia. However, a patient whose consciousness is impaired or who cannot swallow, such as a frail elderly patient, is at risk for hypernatremia. Hypernatremia is caused by:
The nurse can intervene by:
The nurse must be alert to recognize the signs and symptoms of hyperna-tremia. These are:
The nurse should educate the patient to:
Hyponatremia occurs when the patient’s serum sodium is less than 135 mEq/L. There are two reasons why this happens: the patient has increased the volume of water while the sodium concentration remains normal or the patient losses sodium while the water volume remains normal. Hyponatremia is caused by:
The nurse must recognize the following symptoms of hyponatremia:
Hyponatremia is treated by:
The nurse should monitor:
The nurse should educate the patient to:
Calcium is found in equal proportion in intracellular fluid and extracellular fluid. It is combined with phosphate in bone and with protein (albumin) in the serum. A patient receives calcium from ingesting calcium-containing food. Calcium plays a critical role in transmission of nerve impulses, blood clotting, muscle contraction, and the formation of teeth and bone. There is also growing evidence that calcium can help with weight loss.
There are three forms of calcium in serum that can fluctuate among forms depending on changes to the serum pH and/or serum protein (albumin) levels.
The normal serum calcium ranges between 8.5 mg/dL to 10.5 mg/dL. This reflects the calcium level for all three forms of calcium. However, ionized calcium (iC) levels are sometimes reported separately (4-5 mg/dL).
There is a balance between calcium and phosphorus. As serum calcium increases, serum phosphorus decreases. Conversely, as serum calcium decreases, serum phosphorus increases. The level of calcium is regulated by the parathyroid hormone (PTH), calcitonin, and vitamin D.
Low serum calcium causes an increase in the production of PTH. PTH moves calcium out of bone and into the serum. It increases the absorption of calcium from the GI tract. PTH also increases reabsorption of calcium in the kidneys.
Calcitonin is produced by the thyroid gland. Production is increased when there is a high serum calcium level. Calcitonin reverses the action of PTH by increasing the absorption of calcium by bone, decreases calcium absorption in the GI tract, and causes an increase in urine to excrete calcium.
Table : Medications that increase and decrease serum calcium.
Dairy products are the major source of dietary calcium. Eggs, green leafy vegetables, broccoli, legumes, nuts, and whole grains provide smaller amounts. Only about 10% to 30% of the calcium in foods is actually absorbed in the body. Calcium is absorbed in the small intestine. Absorption is influenced by the amount of vitamin D available and the levels of calcium already present in the body.
Hypercalcemia is a condition when the serum calcium level is higher than 10.5 mg/dL indicating there is a higher than normal concentration of calcium. This usually produces a low serum phosphorus level. Hypercalcemia can be caused by:
The nurse should be alert to identify the following signs and symptoms of hypercalcemia:
Treatment is based on the calcium level. The calcium level may need to be lowered quickly because severe hypercalcemia can be life threatening. Treat the underlying cause if known.
Hemodialysis is the most effective method to lower calcium levels in severe cases when kidney function is not normal.
Hypocalcemia occurs when the serum calcium level is lower than 8.5 mg/dL indicating there is a lower than normal concentration of calcium. This usually produces a high serum phosphorus level. Too little calcium intake causes calcium to leave the bone to maintain a normal calcium level. Fractures (broken bones) may occur if a calcium deficit persists because of calcium loss from the bones (demineralization).
Hypocalcemia is caused by:
Patients who experience hypocalcemia may have the following symptoms:
Patients with hypocalcemia can be treated as follows:
Patient education should include information about dietary sources of calcium, the need to maintain physical activity to avoid bone loss, avoid overuse of antacids, and chronic use of laxatives. Patients should be taught to use fruits and fiber for improving bowel elimination. Take oral supplements with meals or after meals to increase absorption.
Magnesium is a sister cation to potassium and is higher in intracellular fluid (ICF). If there is a loss of potassium there is also a loss of magnesium. Magnesium is the coenzyme that metabolizes carbohydrates and proteins and is involved in metabolizing nucleic acids within the cell. Magnesium also has a key role in neuromuscular excitability. The patient acquires magnesium by ingesting magnesium-rich food, where it is absorbed in the GI tract and then excreted in urine.
There is a close relationship between magnesium, potassium, and calcium. PTH (see calcium), which regulates calcium, also influences the magnesium balance. Typically, you’ll assess serum magnesium, calcium, and potassium together. The normal serum magnesium level is between 1.5 mEq/L and 2.5 mEq/L.
Hypermagnesemia is a condition experienced by a patient whose serum magnesium level is greater than 2.5 mEq/L. The major cause of hypermagnesia is an excessive intake of magnesium salts in laxatives such as magnesium sulfate, milk of magnesia, and magnesium citrate. Antacids such as Maalox, Mylanta, and DiGel can also cause hypermagnesemia. Patients who take lithium (antipsychotic medication) are also at risk for hypermagnesemia.
The signs and symptoms of hypermagnesemia are:
Hypomagnesemia happens when the serum magnesium level is less than 1.5 mEq/L. This can be caused by long-term administration of saline infusions which can result in the loss of magnesium and calcium. Diuretics, certain antibiotics, laxatives, and steroids are drug groups that promote magnesium loss. Hypomagnesemia also enhances the action of digitalis and can cause digitalis toxicity.
Patients who have hypomagnesemia may exhibit no signs and symptoms until the serum level approaches 1.0 mEq/L. Signs of severe hypomagnesemia include tetany-like symptoms caused by hyperexcitability (tremors, twitching of the face), ventricular tachycardia that leads to ventricular fibrillation, and hypertension.
Treatment for hypomagnesemia includes:
Keep calcium gluconate available for emergency reversal of hypermagnesemia as a result of overcorrecting hypomagnesemia.
Phosphate is the primary anion inside the cell and plays a key role in the function of red blood cells, muscles, and the nervous system. Phosphate is also involved the acid-base buffering and is involved with metabolizing carbohydrates, proteins, and fats. Most of the body’s phosphate (about 85%) is found in bones. The rest of it is stored in tissues throughout the body.
Phosphorus is acquired by eating phosphorus-rich foods. Phosphorus is absorbed in the GI tract and excreted in urine and a small amount in feces. It is converted to phosphate in the body.
Both phosphate and calcium levels are regulated by parathyroid hormone (PTH). The amount of phosphate in the blood effects the level of calcium in the blood. Both levels are usually measured at the same time. As the serum calcium concentration increases, the concentration of serum phosphorus decreases and conversely as serum phosphorus increases, serum calcium decreases. The nor¬mal range of serum phosphorus is between 2.5 mg/dL and 4.5 mg/dL.
The kidneys regulate the amount of phosphate in the blood. Abnormally high levels of serum phosphate are usually caused by kidney malfunction.
Hyperphosphatemia is the condition exhibited by a patient whose serum phosphate is greater than 4.5 mg/dL, which is caused by:
Unlike hyperkalemia and hypermagnesemia, acute hyperphosphatemia causes few sudden problems. The major effect is to cause hypocalcemia and tetany if serum phosphate rises too rapidly. Calcium can be deposited in the tissues in hyperphosphatemia.
The treatment for acute hyperphosphatemia is administration of phosphate binding salts, calcium, magnesium, and aluminum although aluminum is avoided in renal failure.
Patients who have hyperphosphatemia show the following signs and symptoms:
Treatment for hyperphosphatemia can include:
Hypophosphatemia occurs in a patient’s whose serum phosphate is less than 2.5 mg/dL and is caused by:
The nurse should monitor the patient for the following signs and symptoms of hypophosphatemia:
Hypophosphatemia can be treated by:
Nursing interventions should include:
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