Understanding Fluid Balance in the Human Body

Fluid Balance

• Approximately 60% of a young adult's body weight is water, decreasing to less than 50% in older adults, while infants have 70-80% water content.
• Body fluids contain dissolved substances called solutes, which can be electrolytes (conduct electricity when dissolved in water) or nonelectrolytes (do not conduct electricity).
• Electrolytes include sodium, potassium, calcium, magnesium, acids, and bases.
• Nonelectrolytes include glucose and urea.
• Intracellular fluid (ICF) is fluid inside the cells.
• Extracellular fluid (ECF) is fluid outside the cells, divided into interstitial fluid, intravascular fluid, and transcellular fluid.
• Interstitial fluid surrounds body cells and includes lymph.
• Intravascular fluid (blood plasma) exists within arteries, veins, and capillaries.
• Transcellular fluids are in specific body compartments like cerebrospinal fluid, digestive juices, and synovial fluid.
• The primary control of water in the body is through pressure sensors that stimulate or inhibit antidiuretic hormone (ADH) release from the pituitary gland.
• ADH causes kidneys to retain fluid when vascular fluid pressures decrease and eliminate more water when pressures increase.
• Active transport requires ATP energy to move substances, exemplified by sodium-potassium pumps that move sodium out of cells and potassium into cells.
• Passive transport doesn't require energy expenditure, aided by body movements, and includes diffusion, filtration, and osmosis.
• Diffusion is the movement of a substance from an area of higher concentration to lower concentration.
• Filtration involves water and smaller molecules moving through a semipermeable membrane from high to low pressure.
• Filtration is promoted by hydrostatic pressure differences, important for moving water, nutrients, and waste products in capillaries.
• Osmosis is water movement from lower to higher substance concentration across a semipermeable membrane, driven by osmotic pressure.
• Osmolarity refers to the concentration of substances in body fluids, with normal blood osmolarity between 270 and 300 mOsm/L.
• Tonicity classifies fluids as isotonic (same osmolarity as blood), hypotonic (lower osmolarity than blood), or hypertonic (higher osmolarity than blood).
• Isotonic solutions, like 0.9% saline, are often used for IV therapy.
• Hypotonic solutions cause water to move from the blood into the cells.
• Hypertonic solutions cause water to move from the cells into the bloodstream.
• Water is critical for cellular metabolism, blood volume, temperature regulation, and solute transport, with thirst being the major indicator for needing more water.
• Adults lose about 2,500 mL of fluid daily through sensible (urination) and insensible (perspiration, respiration, stool) losses.
• Older adults are prone to fluid deficits due to diminished thirst reflex and less effective kidney function.

Fluid Imbalances

Dehydration (Fluid Deficit)

• Occurs when there's not enough fluid, especially in the blood (intravascular area), leading to decreased blood volume (hypovolemia).
• Hypovolemia may result from hemorrhage, severe vomiting/diarrhea, draining wounds, or profuse diaphoresis.
• Third spacing, where fluid moves from the intravascular space to the interstitial space, can also cause hypovolemia.
• Conditions that cause third-spacing include burns, liver cirrhosis, and extensive trauma.
• Prevent dehydration by identifying and intervening quickly for high-risk patients like older adults, infants, children, and those with conditions causing fluid loss.
• Encourage adequate hydration with 30 mL/kg/day of fluids for adults, using alternate routes if oral intake is insufficient.
• Older adults may show confusion, lightheadedness, and syncope due to inadequate oxygen supply to the brain.
• Manifestations include thirst, rapid/weak pulse, rapid/shallow respirations, low blood pressure, decreased tear formation, dry skin/mucous membranes, and decreased skin turgor.
• Decreased skin turgor (tenting) is assessed over the sternum or inner thigh.
• Urine output decreases to less than 30 mL per hour, becomes more concentrated, and constipation occurs.
• Weight loss is a major method of evaluating dehydration.
• Complications of untreated dehydration include decreased organ function and failure, leading to death.
• Diagnostic tests show elevated BUN and hematocrit levels, and increased urine specific gravity.
• Therapeutic measures involve replacing fluids (IV therapy with isotonic fluids like normal saline) and resolving the cause.
• Monitor daily weights and I&O, collaborate with healthcare team on fluid intake plans, offer fluids often, correct underlying cause, and avoid overhydration.
• Patient education includes reporting early signs/symptoms of dehydration.

Fluid Excess (Overhydration)

• There is too much fluid in the body.
• Most problems from fluid excess are from too much fluid in the bloodstream or dilution of electrolytes/red blood cells.
• Hypervolemia is excess fluid in the intravascular space.
• Healthy kidneys can compensate for mild to moderate hypervolemia by increasing urinary output.
• Causes include excessive fluid intake (poorly controlled IV therapy, water ingestion), excessive sodium intake, adrenal gland dysfunction, corticosteroid use, kidney failure, heart failure, and syndrome of inappropriate ADH.
• Prevention includes avoiding excessive fluid intake, monitoring IV therapy closely, and monitoring irrigation fluid amounts.
• Signs/symptoms include elevated blood pressure, bounding pulse, increased/labored respirations, distended neck veins, pitting dependent edema, pale/cool skin, increased/diluted urine output, rapid weight gain, moist crackles in lungs, dyspnea, and ascites.
• Acute fluid excess can result in congestive heart failure and pulmonary edema.
• Diagnostic tests show decreased BUN and hematocrit levels, and diminished urine specific gravity.
• Therapeutic measures include semi-Fowler or high Fowler position, oxygen therapy, diuretics (furosemide), and diet therapy (fluid/sodium restriction).
• Monitor fluid I&O, check for edema, auscultate lung sounds, and weigh at-risk patients daily.
• Interventions include reporting increased weight, implementing fluid restriction (as ordered), administering diuretics, and reporting urinary output below 30 mL/hour.
• Patient education includes reinforcing fluid/sodium restrictions.

Electrolyte Imbalances

• Natural minerals in food become electrolytes (ions) in the body through digestion and metabolism.
• Electrolytes are measured in mEq/L or mg/dL.
• Cations have a positive electrical charge; anions have a negative charge.
• Important electrolytes include sodium (Na+), potassium (K+), calcium (Ca2+), and magnesium (Mg2+).
• Concentrations of electrolytes are maintained by pumps in the cell wall.
• Treatment for electrolyte deficit involves oral or IV replacement.
• Treatment for electrolyte excess focuses on eliminating the excess, often via the kidneys, and treating the underlying cause.
• Measures consist of preventing/recognizing electrolyte imbalances, watching for signs in high-risk patients, measuring serum electrolytes, and patient education.

Sodium Imbalances (Na+)

• Normal serum sodium level: 135-145 mEq/L (135-145 mmol/L).
• Sodium maintains serum osmolarity and is important for cell function, especially in the central nervous system.
• The two sodium imbalances are hyponatremia (sodium deficit) and hypernatremia (sodium excess).

Hyponatremia

• Serum sodium level is less than 135 mEq/L.
• Actual decrease results from inadequate sodium intake or excessive sodium loss, pulling water into cells.
• Relative decrease has sodium leave the intravascular space and moves into the interstitial tissues, or plasma volume increases causing a dilutional effect.
• High-risk conditions include NPO status, excessive diaphoresis, diuretics, gastrointestinal suction, syndrome of inappropriate antidiuretic hormone, excessive ingestion of hypotonic fluids, freshwater near-drowning, and decreased aldosterone.
• Patients with fluid deficits have signs and symptoms of dehydration while fluid excess patients have signs/symptoms of fluid excess.
• More severe deficits include mental status changes such as disorientation, agitation, confusion, and personality changes.
• The low sodium and decrease in osmolarity cause water to collect in the brain (cerebral edema) and increase intracranial pressure.
• Weakness, elevated body temperature, tachycardia, nausea, vomiting, and diarrhea may occur.
• Severe hyponatremia can cause seizures, respiratory arrest, coma, and pulmonary edema.
• The primary diagnostic test is a serum sodium level, which registers below 135 mEq/L and decreased serum osmolarity.
• Therapy focuses on resolving the cause of hyponatremia and replacing lost sodium.
• Interventions include IV saline, fluid restriction, diuretics, steroids, strict I&O monitoring, daily weights, and safety measures.

Hypernatremia

• Serum sodium level is above 145 mEq/L.
• There is an actual increase from excessive sodium intake or inability to excrete sodium (kidney failure).
• Or there is a relative increase of decreased fluid in the intravascular space, causing increased percentage of sodium.
• Mild excess can stimulate excitable tissues (muscles/brain neurons), the patient becomes irritable and has tremors.
• Severe excess can result in tissues failing to respond.
• Prevention includes careful regulation of IV fluids.
• Thirst is usually one of the first symptoms to appear.
• Manifestations include mental status changes such as agitation, confusion, and personality changes, and seizures.
• Muscle twitches and unusual contractions may occur. Later, skeletal muscle weakness occurs that can lead to respiratory failure if it affects the diaphragm.
• The patient also has signs and symptoms associated with fluid deficit.
• Severe hypernatremia may cause coma or respiratory arrest as skeletal muscles weaken.
• Diagnostic test includes serum sodium level indicating an increase above the normal level.
• Serum osmolarity may also increase.
• Fluid imbalance is treated first, like fluid replacement without sodium in a patient with dehydration should correct a relative sodium excess.
• Therapy includes treating the underlying cause, a sodium-restricted diet may be prescribed.

Potassium Imbalances (K+)

• Normal level: 3.5 to 5.3 mEq/L (3.5–5.3 mmol/L).
• Is especially important for cardiac, skeletal, and smooth muscle function.
• Hypokalemia (potassium deficit) and hyperkalemia (potassium excess).

Hypokalemia

• Serum potassium level falls below 3.5 mEq/L.
• It results from inadequate intake or excessive loss of potassium through the kidneys.
• Causes include potassium-wasting diuretics (e.g., furosemide and hydrochlorothiazide), corticosteroids (e.g., prednisone), vomiting, diarrhea, prolonged GI suction, major surgery, and hemorrhage.
• Prevention includes potassium supplements with IV fluids, and for patients receiving drugs known to cause hypokalemia, potassium supplements or foods high in potassium may prevent a deficit.
• Manifestations include muscle cramping/fatigue, shallow/ineffective respirations, weak/irregular pulse.
• A major danger, irregular heartbeat (arrhythmia), can cause cardiac arrest.
• Orthostatic (postural) hypotension may be present.
• Other manifestations include changes in mental status followed by lethargy, nausea, vomiting, abdominal distention, and constipation.
• If not corrected, hypokalemia can result in death from arrhythmia, respiratory failure and arrest.
• The primary laboratory test is a serum potassium level, the patient’s ECG may show cardiac arrhythmias.
• In addition to a decrease in the serum potassium level, the patient may have an acid–base imbalance known as metabolic alkalosis.
• The goal of treatment is to replace potassium in the body and resolve the underlying cause of the imbalance.
• With mild to moderate hypokalemia, oral potassium supplements are given.
• With severe hypokalemia, IV potassium supplements are given, potassium should be administered only after the patient has voided and monitored carefully to prevent giving too much potassium.
• Teach the patient about the side effects of oral potassium and precautions associated with potassium administration.

Hyperkalemia

• The serum potassium level exceeds 5.3 mEq/L.
• Causes include overuse of potassium-based salt substitutes or excessive intake of oral or IV potassium supplements.
• Use of potassium-sparing diuretics (e.g., spironolactone [Aldactone]) may contribute to hyperkalemia.
• Patients with kidney failure are at risk because the kidneys cannot excrete potassium.
• Movement of potassium from cells into the blood and other ECF is common in massive tissue trauma and metabolic acidosis.
• Manifestations include muscle twitches and cramps later followed by profound muscular weakness; increased GI motility (diarrhea); slow, irregular heart rate; weak pulse; and decreased blood pressure.
• Prevention includes monitoring serum electrolyte values and the patient’s symptoms and adjusting the dose accordingly.
• Cardiac arrhythmias and respiratory failure can occur in severe hyperkalemia.
• Diagnostic tests include an elevated serum potassium level and ECG changes.
• If the patient has metabolic acidosis, the serum pH falls below 7.35.
• For mild, chronic hyperkalemia, dietary limitation of potassium-rich foods may be helpful. Potassium supplements are discontinued.
• Potassium-wasting diuretics are given to patients with healthy kidneys.
• For patients with kidney problems, a cation exchange resin, such as sodium polystyrene sulfonate, may be administered either orally or rectally.
• Administration of glucose and insulin can facilitate the movement of potassium back into the cells.
• During treatment of moderate to severe hyperkalemia, the patient should be in the hospital on a cardiac monitor.

Calcium Imbalances (Ca2+)

• Normal value for healthy adults is 8.2 to 10.2 mg/dL or 2.1 to 2.6 mmol/L.
• It is needed for proper function of excitable tissues, especially cardiac muscle.
• The two calcium imbalances are hypocalcemia and hypercalcemia.

Hypocalcemia

• Occurs when the serum calcium level falls below 8.2 mg/dL or 2.1 mmol/L.
• Postmenopausal women are most at risk.
• Causes include inadequate absorption of calcium from the intestines (Crohn’s) and insufficient intake of vitamin D.
• Conditions that interfere with the production of parathyroid hormone, such as surgical removal of the thyroid or parathyroid glands, can also cause hypocalcemia.
• Patients with hyperphosphatemia (usually those with kidney failure) often experience hypocalcemia.
• RDA of calcium for adults between 19-50 and men aged 51-70 is 1,000mg. RDA of calcium for women over 50 and men over 70 is 1,200mg.
• Supplements such as calcium carbonate (Tums) can also be taken.
• Chronic signs are usually not diagnosed until the patient breaks a bone.
• Diagnostic tests include ECG and parathyroid hormone levels.
• Acute signs include changes in heart rate, decreased blood pressure, mental status changes, hyperactive deep tendon reflexes, and increased GI motility, including diarrhea and abdominal cramping.
• Testing of Trousseau sign and Chvostek sign, a positive sign indicates hypocalcemia.
• Severe results can lead to neuromuscular irritability to tetany, continuous muscle contraction, the patient may have a sudden laryngospasm blocking air from entering lungs.
• In addition to treating the cause of hypocalcemia, calcium is replaced through foods in table 6.3.
• Supplementation of Vitamin D can also be prescribed.
• Aluminum hydroxide is used to bind the excess phosphate for elimination via the GI tract for patients with hyperphosphatemia.

Hypercalcemia

• Occurs when the serum calcium is above 11 mg/dL, or 5.5 mEq/L.
• Chronic from excessive Vitamin D and calcium intake.
• Excessive causes include Kidney failure, overproduction of parathyroid, cancers.
• Acute caused by invasive cancers.
• Prevented through careful monitoring.
• Symptoms include muscle weakness.
• Acute signs include kidney stones, increased heart rate and blood pressure, and decreased GI motility.
• Severe cases result in respiratory and heart failure.
• Cardiac monitor may need to be employed to analyze ECG.
• Saline infusions and diuretics are administered to promote the excretion of excess calcium.
• Thiazide diuretics are discontinued.
• Drugs such as pamidronate disodium (Aredia), zoledronic acid (Zometa), or calcitonin, which slow calcium movement from bones to the blood, may also be used.
• Hemodialysis, peritoneal dialysis, or ultrafiltration may be necessary to cleanse the blood of excess calcium for those with heart or other severe problems.

Magnesium Imbalances (Mg2+)

• Normal value: 1.6–2.2 mg/dL (0.66–0.91 mmol/L).
• Hypermagnesemia and Hypomagnesemia.

Hypomagnesemia

• Serum magnesium level falls below 1.6 mEq/L.
• Caused by decreased intake or excessive loss of magnesium.
• Intake causes, malnutrition and starvation diets.
• Loss causes, severe diarrhea and Crohn disease.
• One major problem is alcoholism. Causes decreased intake and increases renal excretion.
• Diuretics such as loop and osmotic affect hypomagnesemia.
• Signs that correlate with Hypocalcemia like Trousseau and Chvostek signs.
• Life treating arrhythmias can occur.
• Management to treat Hypomagnesemia includes, treating underlying issues and repleting bodies' supply of magnesium.

Hypermagnesemia

• Increased serum levels beyond 2.2 mEq/L.
• Usually caused by increased intake and decreased renal function.
• Symptoms usually not present unless levels are beyond 4 mg/dL.
• Signs include bradycardia and hypotension.
• When not treated the patient can experience, coma, respiratory failure, and cardiac failure.
• Loop Diuretics such as Furosemide may be administer.
• Dialysis may only be option for those with kidney problems.

Acid-Base Balance

• Cells function best when body fluids/electrolytes are within normal limits.
• Acids release hydrogen ions, with stronger acids releasing more hydrogen ions.
• Hydrochloric acid (HCl) in the stomach is a common acid.
• Bases bind hydrogen ions, with bicarbonate (HCO3−) being a common base.
• Alkali is another word for "base."
• Acids/bases form in the body as part of normal metabolic processes.
• Acids are end products of glucose, fat, and protein metabolism, called fixed acids because they don't change once formed.
• Carbonic acid is a weak acid formed when carbon dioxide combines with water, and can change to bicarbonate/hydrogen.
• Extracellular fluid maintains a balance between acids/bases, measured by pH (0-14 scale, 7 being neutral).
• Normal serum pH: 7.35-7.45 (slightly alkaline), must remain in this range to sustain life.
• Arterial pH lower than 6.9 or higher than 7.8 is usually fatal.
• The body compensates for serum pH changes via cellular buffers, lungs, and kidneys.
• Cellular buffers (proteins, hemoglobin, bicarbonate, phosphates) act as sponges to soak up or release hydrogen ions.
• Lungs "blow off" additional carbon dioxide through rapid, deep breathing when blood is too acidic.
• Lungs conserve carbon dioxide through shallow respirations when blood is too alkaline.
• Kidneys regulate bicarbonate amount, reabsorbing additional bicarbonate when serum pH lowers and excreting additional bicarbonate when serum pH increases, they also buffer pH by forming acids and ammonium (a base).
• Acidosis or alkalosis that is corrected for by the body is referred to as compensated.

Acid-Base Imbalances

• Caused by acute/chronic illnesses or conditions, with primary treatment managing the underlying cause.
• Nurses identify at-risk patients and monitor laboratory test values for significant changes.
• Arterial blood gases (ABGs) are used to evaluate acid–base balance.
• Blood is sampled from an artery rather than a vein.
• Two broad types of acid-base imbalance include acidosis and alkalosis which can be acute or chronic.

Acidosis

• The serum pH level falls below 7.35, the blood becomes more acidic than normal.
• Two types: respiratory acidosis and metabolic acidosis are caused by too much acid or too little base in the body.

Alkalosis

• The serum pH level increases above 7.45, the blood becomes more alkaline or basic.
• Two types: respiratory alkalosis and metabolic alkalosis caused by too little acid in the body or too much base.