Body fluids and electrolytes play an important role in maintaining homeostasis, the stable internal environment of the body.¹ Body fluids are in constant motion transporting nutrients, electrolytes, and oxygen to cells and carrying waste products away from cells. The body uses a number of adaptive responses associated with these activities to keep the composition and volume of body fluids and electrolytes within the narrow limits of normal to maintain homeostasis and promote health.

Many diseases and their treatments can affect fluid and electrolyte balance. For example, a patient with metastatic breast or lung cancer may develop hypercalcemia because of bone destruction from tumor invasion. Chemotherapy prescribed to treat the cancer may result in nausea and vomiting and, subsequently, dehydration and acid-base imbalances. When correcting dehydration with IV fluids, the patient requires close monitoring to prevent fluid overload.

It is important for you to anticipate the potential for alterations in fluid and electrolyte balance associated with certain disorders and medical therapies, recognize the signs and symptoms of imbalances, and intervene with the appropriate action. This chapter describes the (1) normal control of fluids, electrolytes, and acid-base balance; (2) conditions that disrupt homeostasis and resultant manifestations; and (3) actions that the health care provider and you can take to prevent fluid, electrolyte, and acid-base imbalances and restore homeostasis.

Water Content of the Body

Water is the primary component of the body, accounting for approximately 50% to 60% of body weight in the adult. The water content varies with gender, body mass, and age (Fig. 17-1). The percentage of body weight that is composed of water is generally greater in men than in women because men tend to have more lean body mass. The more fat present in the body, the less the total water content. Therefore obese individuals have a lower percentage of body water than slender people do. Older adults, with less muscle mass and more fat content, have less body water for this same reason. In the older adult, body water content averages 45% to 55% of body weight, leaving them at a higher risk for fluid-related problems than young adults.

FIG. 17-1 Body water over the life span.

Body Fluid Compartments

The two fluid compartments in the body are the intracellular space (inside the cells) and the extracellular space (outside the cells) (Fig. 17-2). Approximately two thirds of the body water is located within cells and is termed intracellular fluid (ICF); ICF constitutes approximately 40% of body weight of an adult. The body of a 70-kg young man would contain approximately 42 L of water, of which 28 L would be located within cells.

FIG. 17-2 Relative volumes of three body fluids. Values represent fluid distribution in a young male adult.

The extracellular fluid (ECF) consists of interstitial fluid (the fluid in the spaces between cells), plasma (the liquid part of blood), and transcellular fluid (a very small amount of fluid contained within specialized cavities of the body). Transcellular fluids include cerebrospinal fluid; fluid in the gastrointestinal (GI) tract; and pleural, synovial, peritoneal, intraocular, and pericardial fluid. ECF consists of one third of the body water; this would amount to about 14 L in a 70-kg man. About 20% of ECF is in the intravascular space as plasma (3 L in a 70-kg man), and 70% is in the interstitial space (10 L in a 70-kg man). The fluid in the transcellular spaces totals about 1 L at any given time. However, because 3 to 6 L of fluid is secreted into and reabsorbed from the GI tract every day, loss of this fluid from vomiting or diarrhea can produce serious fluid and electrolyte imbalances.

Electrolyte Composition of Fluid Compartments

Electrolyte composition varies between ECF and ICF. The overall concentration of electrolytes is approximately the same in the two compartments. However, concentrations of specific ions differ greatly (Fig. 17-3). In ECF the main cation is sodium, with small amounts of potassium, calcium, and magnesium. The primary ECF anion is chloride, with small amounts of bicarbonate, sulfate, and phosphate anions. In ICF the most prevalent cation is potassium, with small amounts of magnesium and sodium. The prevalent ICF anion is phosphate, with some protein and a small amount of bicarbonate. (Normal serum electrolyte values are presented in Table 17-1.)

TABLE 17-1

NORMAL SERUM ELECTROLYTE VALUES

Electrolyte	Reference Interval
Anions
Bicarbonate (HCO₃⁻)	22-26 mEq/L (22-26 mmol/L)
Chloride (Cl⁻)	96-106 mEq/L (96-106 mmol/L)
Phosphate (PO₄³⁻)*	2.4-4.4 mg/dL (0.78-1.42 mmol/L)
Cations
Potassium (K⁺)	3.5-5.0 mEq/L (3.5-5.0 mmol/L)
Magnesium (Mg²⁺)	1.5-2.5 mEq/L (0.75-1.25 mmol/L)
Sodium (Na⁺)	135-145 mEq/L (135-145 mmol/L)
Calcium (Ca²⁺) (total)	8.6-10.2 mg/dL (2.15-2.55 mmol/L)
Calcium (ionized)	4.6-5.3 mg/dL (1.16-1.32 mmol/L)

^*The majority of the phosphorus (P) in the body is found as phosphate (PO₄³⁻). The terms are used interchangeably in this text.

Mechanisms Controlling Fluid and Electrolyte Movement

The movement of electrolytes and water between ICF and ECF involves many different processes, including simple diffusion, facilitated diffusion, and active transport. Water moves as driven by two forces: hydrostatic pressure and osmotic pressure.

Diffusion

Diffusion is the movement of molecules from an area of high concentration to one of low concentration (Fig. 17-4). It occurs in liquids, gases, and solids. Net movement of molecules across a membrane stops when the concentrations are equal in both areas. The membrane separating the two areas must be permeable to the diffusing substance for the process to occur. Simple diffusion requires no external energy.

Facilitated Diffusion

Facilitated diffusion involves the use of a protein carrier in the cell membrane. The protein carrier combines with a molecule, especially one too large to pass easily through the cell membrane, and assists in moving the molecule across the membrane from an area of high concentration to one of low concentration. Like simple diffusion, facilitated diffusion is passive and requires no energy. Glucose transport into the cell is an example of facilitated diffusion. The large glucose molecule must combine with a carrier molecule to be able to cross the cell membrane and enter most cells.

Active Transport

Active transport is a process in which molecules move against the concentration gradient. External energy is required for this process. An example is the sodium-potassium pump. The concentrations of sodium and potassium differ greatly intracellularly and extracellularly (see Fig. 17-3). To maintain this concentration difference, the cell uses active transport to move sodium out of the cell and potassium into the cell (Fig. 17-5). The energy source for this mechanism is adenosine triphosphate (ATP), produced in the cell’s mitochondria.

Osmosis

Osmosis is the movement of water “down” a concentration gradient, that is, from a region of low solute concentration to one of high solute concentration, across a semipermeable membrane.² Imagine a chamber with two compartments separated by a semipermeable membrane, one that allows only the movement of water (Fig. 17-6). Water will move from the less concentrated side (has more water) to the more concentrated side of the chamber water (has less water). Osmosis requires no outside energy sources and stops when the concentration differences disappear or when hydrostatic pressure builds and is sufficient to oppose any further movement of water.

Whenever dissolved substances are contained in a space with a semipermeable membrane, they can pull water into the space by osmosis. The concentration of the solution determines the strength of the osmotic pull. The higher the concentration, the greater the solution’s pulling, or osmotic pressure. Osmotic pressure is measured in milliosmoles (mOsm) and may be expressed as either fluid osmolarity or fluid osmolality. Although the terms osmolarity and osmolality are often used interchangeably, they are different measurements. 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 test typically performed to evaluate the concentration of plasma and urine.²

Measurement of Osmolality.

Osmolality is approximately the same in the various body fluid spaces. Determining osmolality is important because it indicates the body’s water balance. To assess the state of the body’s water balance, one can measure or estimate plasma osmolality. Normal plasma osmolality is between 275 and 295 mOsm/kg. A value greater than 295 mOsm/kg indicates that the concentration of particles is too great or that the water content is too little. This condition is termed water deficit. A value less than 275 mOsm/kg indicates too little solute for the amount of water or too much water for the amount of solute. This condition is termed water excess. Both conditions are clinically significant. Because the major determinants of plasma osmolality are sodium and glucose, one can calculate the effective plasma osmolality based on the concentrations of those substances.

Osmolality of urine can range from 100 to 1300 mOsm/kg, depending on fluid intake and the amount of antidiuretic hormone (ADH) in circulation and the renal response to it.

Osmotic Movement of Fluids.

The osmolality or tonicity of the fluid surrounding the cells affects them. Fluids with the same osmolality as the cell interior are termed isotonic. Normally, ECF and ICF are isotonic to one another, so no net movement of water occurs.

Changes in the osmolality of ECF alter the volume of cells. Solutions in which the solutes are less concentrated than in the cells are termed hypotonic (hypoosmolar). If a cell is surrounded by hypotonic fluid, water moves into the cell, causing it to swell and possibly to burst. Fluids with solutes more concentrated than in cells, or an increased osmolality, are termed hypertonic (hyperosmolar). If hypertonic fluid surrounds a cell, water leaves the cell to dilute ECF; the cell shrinks and may eventually die (Fig. 17-7).

FIG. 17-7 Effects of water status on red blood cells. A, Hypotonic solution (H₂O excess) results in cellular swelling. B, Isotonic solution (normal H₂O balance) results in no change. C, Hypertonic solution (H₂O deficit) results in cellular shrinking.

Hydrostatic Pressure

Hydrostatic pressure is the force within a fluid compartment. In the blood vessels, hydrostatic pressure is the blood pressure generated by the contraction of the heart. Hydrostatic pressure in the vascular system gradually decreases as the blood moves through the arteries until it is about 30 mm Hg in the capillary bed. 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

Oncotic pressure (colloidal osmotic pressure) is the osmotic pressure caused by plasma colloids in solution. The major colloid in the vascular system contributing to the total osmotic pressure is protein. Plasma has substantial amounts of protein, whereas the interstitial space has very little. The plasma protein molecules attract water, pulling fluid from the tissue space to the vascular space. Under normal conditions, plasma oncotic pressure is approximately 25 mm Hg. The small amount of protein found in the interstitial space exerts an oncotic pressure of approximately 1 mm Hg.

Fluid Movement in Capillaries

As plasma flows through the capillary bed, four factors determine if fluid moves out of the capillary and into the interstitial space or if fluid moves back into the capillary from the interstitial space. The amount and direction of movement are determined by the interaction of (1) capillary hydrostatic pressure, (2) plasma oncotic pressure, (3) interstitial hydrostatic pressure, and (4) interstitial oncotic pressure.

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. At the arterial end of the capillary, capillary hydrostatic pressure exceeds plasma oncotic pressure, and fluid moves into the interstitial space. At the venous end of the capillary, the capillary hydrostatic pressure is lower than plasma oncotic pressure, drawing fluid back into the capillary by the oncotic pressure created by plasma proteins (Fig. 17-8).

FIG. 17-8 Dynamics of fluid exchange between a capillary and tissue. An equilibrium exists between forces filtering fluid out of the capillary and forces absorbing fluid back into the capillary. Note that the hydrostatic pressure is greater at the arterial end of the capillary than at the venous end. The net effect of pressures at the arterial end of the capillary causes a movement of fluid into the tissue. At the venous end of the capillary, there is net movement of fluid back into the capillary.

Fluid Shifts

If capillary or interstitial pressures change, fluid may abnormally shift from one compartment to another, resulting in edema or dehydration.

Shifts of Plasma to Interstitial Fluid.

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.

Elevation of Venous Hydrostatic Pressure.

Increasing the pressure at the venous end of the capillary inhibits fluid movement back into the capillary, which results in edema. Causes of increased venous pressure include fluid overload, heart failure, liver failure, obstruction of venous return to the heart (e.g., tourniquets, restrictive clothing, venous thrombosis), and venous insufficiency (e.g., varicose veins).

Decrease in Plasma Oncotic Pressure.

Fluid remains in the interstitial space if the plasma oncotic pressure is too low to draw fluid back into the capillary. Low plasma protein content decreases oncotic pressure. This can result from excessive protein loss (renal disorders), deficient protein synthesis (liver disease), and deficient protein intake (malnutrition).

Elevation of Interstitial Oncotic Pressure.

Trauma, burns, and inflammation can damage capillary walls and allow plasma proteins to accumulate in the interstitial space. This increases interstitial oncotic pressure, draws fluid into the interstitial space, and holds it there.

Shifts of Interstitial Fluid to Plasma.

An increase in the plasma osmotic or oncotic pressure draws fluid into the plasma from the interstitial space. This could happen with administration of colloids, dextran, mannitol, or hypertonic solutions. Increasing the tissue hydrostatic pressure is another way of causing a shift of fluid into plasma. Wearing elastic compression gradient stockings or hose to decrease peripheral edema is a therapeutic application of this effect.

Fluid Spacing

Fluid spacing is a term used to describe the distribution of body water. First spacing describes the normal distribution of fluid in ICF and ECF compartments. Second spacing refers to an abnormal accumulation of interstitial fluid (i.e., edema). Third spacing occurs when fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ECF. Third-spaced fluid is trapped and unavailable for functional use. Examples of third spacing are ascites; sequestration of fluid in the abdominal cavity with peritonitis; and edema associated with burns, trauma, or sepsis.³

Regulation of Water Balance

Hypothalamic-Pituitary Regulation

Water balance is maintained via the finely tuned balance of water intake and excretion. Water ingestion will equal water loss in the individual who has free access to water, a normal thirst and ADH mechanism, and normally functioning kidneys.

An intact thirst mechanism is critical because it is the primary protection against the development of hyperosmolality. Osmoreceptors in the hypothalamus sense a body fluid deficit or increase in plasma osmolality, which in turn stimulates thirst and ADH release. Thirst causes the patient to drink water. The distal tubules and collecting ducts in the kidneys respond to ADH by becoming more permeable to water. The result is increased water reabsorption from the tubular filtrate into the blood and decreased excretion in the urine. Together these factors result in increased free water in the body and decreased plasma osmolality.

The patient who cannot recognize or act on the sensation of thirst is at risk for fluid deficit and hyperosmolality. Other factors that stimulate ADH release include stress, nausea, nicotine, and morphine. A decreased plasma osmolality or water excess suppresses secretion of ADH, resulting in urinary excretion of water. It is common for the postoperative patient to have a lower plasma osmolality, possibly because of the stress of surgery and opioid analgesia. Social and psychologic factors not related to fluid balance also affect the desire to consume fluids. A dry mouth will cause the patient to drink, even when there is no measurable body water deficit.

Renal Regulation

The kidneys are the primary organs for regulating fluid and electrolyte balance (see Chapter 45). The kidneys regulate water balance by adjusting urine volume and the urinary excretion of most electrolytes to maintain a balance between overall intake and output. The kidneys filter the total plasma volume many times each day. In the average adult the kidneys reabsorb 99% of this filtrate, producing approximately 1.5 L of urine per day. As the filtrate moves through the renal tubules, selective reabsorption of water and electrolytes and secretion of electrolytes result in the production of urine that is greatly different in composition and concentration from plasma. This process helps maintain normal plasma osmolality, electrolyte balance, blood volume, and acid-base balance. The renal tubules are the site for the actions of ADH and aldosterone.

With severely impaired renal function, the kidneys cannot maintain fluid and electrolyte balance. This condition results in edema, potassium and phosphorus retention, acidosis, and other electrolyte imbalances (see Chapter 47).

Adrenal Cortical Regulation

Glucocorticoids and mineralocorticoids secreted by the adrenal cortex help regulate both water and electrolytes. The glucocorticoids (e.g., cortisol) primarily have an antiinflammatory effect and increase serum glucose levels, whereas the mineralocorticoids (e.g., aldosterone) enhance sodium retention and potassium excretion (Fig. 17-9). When sodium is reabsorbed, water follows because of osmotic changes.

FIG. 17-9 Factors affecting aldosterone secretion. *ACTH,* Adrenocorticotropic hormone.

Cortisol is the most abundant glucocorticoid. In large doses, cortisol has both glucocorticoid (glucose elevating and antiinflammatory) and mineralocorticoid (sodium-retention) effects. Normally cortisol secretion is in a diurnal or circadian pattern. Increased cortisol secretion occurs in response to physical and psychologic stress, affecting many body functions, including fluid and electrolyte balance (Fig. 17-10).

FIG. 17-10 Effects of stress on fluid and electrolyte balance. *ACTH,* Adrenocorticotropic hormone; *ADH,* antidiuretic hormone; *CRH,* corticotropin-releasing hormone.

Aldosterone is a mineralocorticoid with potent sodium-retaining and potassium-excreting capabilities. Decreased renal perfusion or decreased sodium delivery to the distal portion of the renal tubule activates the renin-angiotensin-aldosterone system (RAAS), which results in aldosterone secretion (see Fig. 45-4). In addition to the RAAS, increased plasma potassium, decreased plasma sodium, and adrenocorticotropic hormone (ACTH) from the anterior pituitary act directly on the adrenal cortex to stimulate the secretion of aldosterone (see Fig. 17-9).

Cardiac Regulation

Natriuretic peptides, including atrial natriuretic peptide (ANP) and b-type natriuretic peptide (BNP), are hormones produced by cardiomyocytes. They are natural antagonists to the RAAS. They are produced in response to increased atrial pressure (increased volume, such as occurs in heart failure) and high serum sodium levels. They suppress secretion of aldosterone, renin, and ADH, and the action of angiotensin II. In the renal tubules these peptides promote excretion of sodium and water, resulting in a decrease in blood volume and blood pressure.

Gastrointestinal Regulation

Daily water intake and output are normally between 2000 and 3000 mL (Table 17-2). Oral intake of fluids accounts for most of the water intake. Water intake also includes water from food metabolism and water present in solid foods. Lean meat is approximately 70% water, whereas the water content of many fruits and vegetables approaches 100%.

TABLE 17-2

NORMAL FLUID BALANCE IN THE ADULT

In addition to oral intake, the GI tract normally secretes approximately 8000 mL of digestive fluids each day. Most of this fluid is reabsorbed in the GI tract; only a small amount is normally eliminated in feces. Diarrhea and vomiting, which prevent GI reabsorption of this secreted fluid, can lead to significant fluid and electrolyte loss.

Insensible Water Loss

Insensible water loss, which is invisible vaporization from the lungs and skin, assists in regulating body temperature. Normally, about 600 to 900 mL/day is lost. Accelerated body metabolism, which occurs with increased body temperature and exercise, increases the amount of water loss.

Do not confuse water loss through the skin with the vaporization of water excreted by sweat glands. Insensible perspiration causes only water loss. Excessive sweating (sensible perspiration) caused by exercise, fever, or high environmental temperatures may lead to large losses of water and electrolytes.

Gerontologic Considerations

Fluid and Electrolytes

The older adult experiences normal physiologic changes with aging that increase susceptibility to fluid and electrolyte imbalances. Structural changes to the kidneys and a decrease in the renal blood flow lead to decreased glomerular filtration rate, decreased creatinine clearance, and loss of the ability to concentrate urine and conserve water. Hormonal changes include a decrease in renin and aldosterone and an increase in ADH and ANP.⁴ Loss of subcutaneous tissue and thinning of the dermis lead to increased loss of moisture through the skin and an inability to respond to heat or cold quickly.

Older adults experience a decrease in the thirst mechanism, resulting in decreased fluid intake despite increases in osmolality and serum sodium level. Older adults, especially if they are ill, are at increased risk of free-water loss and subsequent development of hypernatremia secondary to impairment of the thirst mechanism and barriers to obtaining fluids to drink.⁵

Healthy older adults usually consume adequate fluids to remain well hydrated. However, functional changes may occur that affect the ability to independently obtain fluids. For example, musculoskeletal changes, such as stiffness of the hands and fingers, can lead to a decreased ability to hold a glass or cup. Mental status changes, such as confusion or disorientation, or changes in ambulation status may lead to a decreased ability to obtain fluids. To reduce incontinent episodes, the older adult may intentionally restrict fluid intake.

You should not automatically attribute older patients’ fluid and electrolyte problems to the natural processes of aging. Adapt your assessment and nursing interventions to account for these physiologic and functional changes. Suggestions for alterations in nursing care for the older adult are presented throughout this chapter.

Fluid and Electrolyte Imbalances

Fluid and electrolyte imbalances occur to some degree in most patients with a major illness or injury because illness disrupts the normal homeostatic mechanism. Some fluid and electrolyte imbalances are directly caused by illness or disease (e.g., burns, heart failure). At other times, therapeutic measures (e.g., IV fluid replacement, diuretics) cause or contribute to fluid and electrolyte imbalances. Perioperative patients are at risk for the development of fluid and electrolyte imbalances because of fluid restrictions, blood or fluid loss, and the stress of surgery.⁶

Imbalances are commonly classified as deficits or excesses. Although each imbalance is discussed separately in this chapter, it is common for more than one imbalance to occur in the same patient. For example, a patient with prolonged nasogastric suction will lose sodium, potassium, hydrogen, and chloride ions. These imbalances may result in a deficiency of both sodium and potassium, a fluid volume deficit, and metabolic alkalosis caused by loss of hydrochloric acid.

Extracellular Fluid Volume Imbalances

ECF volume deficit (hypovolemia) and ECF volume excess (hypervolemia) are common clinical conditions. ECF volume imbalances are typically accompanied by one or more electrolyte imbalances, particularly changes in the serum sodium level.

Fluid Volume Deficit

Fluid volume deficit can occur with abnormal loss of body fluids (e.g., diarrhea, fistula drainage, hemorrhage, polyuria), inadequate intake, or a shift of fluid from plasma into interstitial fluid. The term fluid volume deficit is not interchangeable with the term dehydration. Dehydration refers to loss of pure water alone without a corresponding loss of sodium. Causes and clinical manifestations of fluid volume deficit are listed in Table 17-3.

TABLE 17-3

EXTRACELLULAR FLUID IMBALANCES: CAUSES AND CLINICAL MANIFESTATIONS

ECF Volume Deficit	ECF Volume Excess
Causes
• ↑ Insensible water loss or perspiration (high fever, heatstroke) • Diabetes insipidus • Osmotic diuresis • Hemorrhage • GI losses: vomiting, NG suction, diarrhea, fistula drainage • Overuse of diuretics • Inadequate fluid intake • Third-space fluid shifts: burns, intestinal obstruction	• Excessive isotonic or hypotonic IV fluids • Heart failure • Renal failure • Primary polydipsia • SIADH • Cushing syndrome • Long-term use of corticosteroids
Clinical Manifestations
• Restlessness, drowsiness, lethargy, confusion • Thirst, dry mucous membranes • Decreased skin turgor, ↓ capillary refill • Postural hypotension, ↑ pulse, ↓ CVP • ↓ Urine output, concentrated urine • ↑ Respiratory rate • Weakness, dizziness • Weight loss • Seizures, coma	• Headache, confusion, lethargy • Peripheral edema • Jugular venous distention • Bounding pulse, ↑ BP, ↑ CVP • Polyuria (with normal renal function) • Dyspnea, crackles, pulmonary edema • Muscle spasms • Weight gain • Seizures, coma

CVP, Central venous pressure; ECF, extracellular fluid; SIADH, syndrome of inappropriate antidiuretic hormone.

Collaborative Care

The goal of treatment for fluid volume deficit is to correct the underlying cause and to replace both water and any needed electrolytes. Balanced IV solutions, such as lactated Ringer’s solution, are usually given. Isotonic (0.9%) sodium chloride is used when rapid volume replacement is indicated. Blood is administered when volume loss is due to blood loss.

Fluid Volume Excess

Fluid volume excess may result from excessive intake of fluids, abnormal retention of fluids (e.g., heart failure, renal failure), or a shift of fluid from interstitial fluid into plasma fluid. Although fluid shifts between the interstitial space and plasma do not alter the overall volume of ECF, these shifts result in changes in the intravascular volume. Causes and clinical manifestations of fluid volume excess are listed in Table 17-3.

Collaborative Care

The goal of treatment for fluid volume excess is removing fluid without producing abnormal changes in the electrolyte composition or osmolality of ECF. The primary cause must be identified and treated. Diuretics and fluid restriction are the primary forms of therapy. Restriction of sodium intake may also be indicated. If the fluid excess leads to ascites or pleural effusion, an abdominal paracentesis or thoracentesis may be necessary.

Nursing Management Extracellular Fluid Volume Imbalances

Nursing Diagnoses

Nursing diagnoses and collaborative problems for the patient with fluid imbalances include, but are not limited to, the following:

ECF volume deficit:

• Deficient fluid volume related to excessive ECF losses or decreased fluid intake

• Decreased cardiac output related to excessive ECF losses or decreased fluid intake

• Risk for deficient fluid volume related to excessive ECF losses or decreased fluid intake

• Potential complication: hypovolemic shock

ECF volume excess:

• Excess fluid volume related to increased water and/or sodium retention

• Impaired gas exchange related to water retention leading to pulmonary edema

• Risk for impaired skin integrity related to edema

• Activity intolerance related to increased water retention, fatigue, and weakness

• Disturbed body image related to altered body appearance secondary to edema

• Potential complications: pulmonary edema, ascites

Nursing Implementation

Intake and Output.

The use of 24-hour intake and output records gives valuable information regarding fluid and electrolyte problems. An accurately recorded intake-and-output flow sheet can identify sources of excessive intake or fluid losses. Intake should include oral, IV, and tube feedings and retained irrigants. Output includes urine, excess perspiration, wound or tube drainage, vomitus, and diarrhea. Estimate fluid loss from wounds and perspiration. Measure the urine specific gravity according to agency policy. Readings of greater than 1.025 indicate concentrated urine, whereas those of less than 1.010 indicate dilute urine.

Cardiovascular Changes.

Monitoring the patient for cardiovascular changes is necessary to prevent or detect complications from fluid and electrolyte imbalances. Signs and symptoms of ECF volume excess and deficit are reflected in changes in blood pressure, pulse force, and jugular venous distention. In fluid volume excess the pulse is full, bounding, and not easily obliterated. Increased volume causes distended neck veins (jugular venous distention) and increased blood pressure.

In mild to moderate fluid volume deficit, compensatory mechanisms include sympathetic nervous system stimulation of the heart and peripheral vasoconstriction. Stimulation of the heart increases the heart rate and, combined with vasoconstriction, maintains the blood pressure within normal limits. A change in position from lying to sitting or standing may elicit a further increase in the heart rate or a decrease in the blood pressure (orthostatic hypotension). If vasoconstriction and tachycardia provide inadequate compensation, hypotension occurs when the patient is recumbent. Severe fluid volume deficit can cause flattened neck veins and a weak, thready pulse that is easily obliterated. Severe, untreated fluid deficit will result in shock.

Respiratory Changes.

Both fluid excess and fluid deficit affect respiratory status. ECF excess can result in pulmonary congestion and pulmonary edema as increased hydrostatic pressure in the pulmonary vessels forces fluid into the alveoli. The patient will experience shortness of breath and moist crackles on auscultation. The patient with ECF deficit will demonstrate an increased respiratory rate because of decreased tissue perfusion and resultant hypoxia.

Neurologic Changes.

Changes in neurologic function may occur with fluid volume excesses or deficits. ECF excess may result in cerebral edema from increased hydrostatic pressure in cerebral vessels. Alternatively, profound volume depletion may cause an alteration in sensorium secondary to reduced cerebral tissue perfusion.

Assessment of neurologic function includes evaluation of (1) the level of consciousness, which includes responses to verbal and painful stimuli and determination of a person’s orientation to time, place, and person; (2) pupillary response to light and equality of pupil size; and (3) voluntary movement of the extremities, degree of muscle strength, and reflexes. Nursing care focuses on maintaining patient safety.

Daily Weights.

Accurate daily weights provide the easiest measurement of volume status. An increase of 1 kg (2.2 lb) is equal to 1000 mL (1 L) of fluid retention (provided the person has maintained usual dietary intake or has not been on nothing-by-mouth [NPO] status). Obtain the weight under standardized conditions, that is, weigh the patient at the same time every day, wearing the same garments, and on the same carefully calibrated scale. Remove excess bedding and empty all drainage bags before the weighing. If the patient has items present that are not there every day, such as bulky dressings or tubes, note this along with the weight.

Skin Assessment and Care.

Detect clues to ECF volume deficit and excess by inspecting the skin. Examine the skin for turgor and mobility. Normally a fold of skin, when pinched, will readily move and, on release, rapidly return to its former position. Skin areas over the sternum, abdomen, and anterior forearm are the usual sites for evaluation of tissue turgor (Fig. 17-11). In older people, decreased skin turgor is less predictive of fluid deficit because of the loss of tissue elasticity.⁴ In ECF volume deficit, skin turgor is diminished, and there is a lag in the pinched skinfold’s return to its original state (referred to as tenting).

FIG. 17-11 Assessment of skin turgor. A and B, When normal skin is pinched, it resumes shape in seconds. C, If the skin remains wrinkled for 20 to 30 seconds, the patient has poor skin turgor.

The skin may be cool and moist if there is vasoconstriction to compensate for the decreased fluid volume. Mild hypovolemia usually does not stimulate this compensatory response. Consequently, the skin will be warm and dry. Volume deficit may also cause the skin to appear dry and wrinkled. These signs may be difficult to evaluate in the older adult because the patient’s skin may be normally dry, wrinkled, and nonelastic. Oral mucous membranes will be dry, the tongue may be furrowed, and the individual often complains of thirst. Routine oral care is critical for the comfort of a patient who is dehydrated or fluid restricted for management of fluid volume excess.

Edematous skin may feel cool because of fluid accumulation and a decrease in blood flow secondary to the pressure of the fluid. The fluid can also stretch the skin, causing it to feel taut and hard. Assess edema by pressing with a thumb or forefinger over the edematous area. A grading scale is used to standardize the description if an indentation (ranging from 1+ [slight edema; 2-mm indentation] to 4+ [pitting edema; 8-mm indentation]) remains when pressure is released. Evaluate for edema in areas where soft tissues overlie a bone, with preferred sites being the tibia, fibula, and sacrum.

Good skin care for the person with ECF volume excess or deficit is important. Protect edematous tissues from extremes of heat and cold, prolonged pressure, and trauma. Frequent skin care and changes in position will prevent skin breakdown. Elevate edematous extremities to promote venous return and fluid reabsorption. Dehydrated skin needs frequent care without the use of soap. Applying moisturizing creams or oils increases moisture retention and stimulates circulation.

Other Nursing Measures.

Carefully monitor the rates of infusion of IV fluid solutions. Be cautious about any attempts to “catch up,” particularly when large volumes of fluid or certain electrolytes are involved. This is especially true in patients with cardiac, renal, or neurologic problems. Patients receiving tube feedings need supplementary water added to their enteral formula. The amount of additional water depends on the osmolarity of the feeding and the patient’s condition.

Do not allow the patient with nasogastric suction to drink water because it will increase the loss of electrolytes. Occasionally the patient may be given small amounts of ice chips to suck. Irrigate nasogastric tubes with isotonic saline solution, not with water. Water causes diffusion of electrolytes into the gastric lumen from mucosal cells. The suction then removes the electrolytes, increasing the risk of electrolyte imbalances.

Nurses in hospitals and long-term care facilities should encourage and help the older or debilitated patient to maintain adequate oral intake. Assess the patient’s ability to obtain adequate fluids independently, express thirst, and swallow effectively.⁴ Fluids should be easily accessible. Assist older adults with physical limitations, such as arthritis, to open and hold containers. A variety of types of fluids should be available, and assess for individual preferences. Serve fluids at the temperature preferred by the patient. Seventy percent to 80% of the daily intake of fluids should be with meals, with fluid supplements between meals. Older adults may choose to decrease or eliminate fluids 2 hours before bedtime to decrease nocturia or incontinence. The unconscious or cognitively impaired patient is at increased risk because of an inability to express thirst and act on it. In these patients, accurately document fluid intake and losses and carefully evaluate the adequacy of intake and output.⁴

Sodium Imbalances

Sodium, the main cation of ECF, plays a major role in maintaining the concentration and volume of ECF and influencing water distribution between ECF and ICF. Sodium plays an important role in the generation and transmission of nerve impulses, muscle contractility, and the regulation of acid-base balance.

Because sodium is the primary determinant of ECF osmolality, sodium imbalances are typically associated with parallel changes in osmolality. Serum sodium is measured in milliequivalents per liter (mEq/L) or millimoles per liter (mmol/L). The serum sodium level reflects the ratio of sodium to water, not necessarily the loss or gain of sodium. Changes in the serum sodium level may reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two. Sodium imbalances are typically associated with imbalances in ECF volume (Figs. 17-12 and 17-13).

FIG. 17-12 Differential assessment of extracellular fluid *(ECF)* volume.

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. The kidneys regulate the ECF concentration of sodium by excreting or retaining water under the influence of ADH. Aldosterone also plays a role in sodium regulation by promoting sodium reabsorption from the renal tubules.

Hypernatremia

Hypernatremia, an elevated serum sodium, may occur with water loss or sodium gain. Because sodium is the major determinant of the ECF osmolality, hypernatremia causes hyperosmolality. In turn, ECF hyperosmolality causes a shift of water out of the cells, which leads to cellular dehydration. As discussed earlier, the primary protection against the development of hyperosmolality is thirst. Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. Hypernatremia secondary to water deficiency is often the result of an impaired level of consciousness or an inability to obtain fluids.

Several clinical states can produce hypernatremia from water loss (Table 17-4). A deficiency in the synthesis or release of ADH from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ADH (nephrogenic diabetes insipidus) can result in profound diuresis, thus producing a water deficit and hypernatremia. Hyperosmolality with osmotic diuresis can result from administration of concentrated hyperosmolar tube feedings and hyperglycemia associated with uncontrolled diabetes mellitus. Other causes of hypernatremia include excessive sweating and increased sensible losses from high fever.

TABLE 17-4

SODIUM IMBALANCES: CAUSES AND CLINICAL MANIFESTATIONS

Hypernatremia (Na⁺ >145 mEq/L [mmol/L])	Hyponatremia (Na⁺ <135 mEq/L [mmol/L])
Causes
*Excessive Sodium Intake*	*Excessive Sodium Loss*
• IV fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarbonate • Hypertonic tube feedings without water supplements • Near-drowning in salt water	• GI losses: diarrhea, vomiting, fistulas, NG suction • Renal losses: diuretics, adrenal insufficiency, Na⁺ wasting renal disease • Skin losses: burns, wound drainage
*Inadequate Water Intake*	*Inadequate Sodium Intake*
• Unconscious or cognitively impaired individuals	• Fasting diets
*Excessive Water Loss (↑ sodium concentration)*	*Excessive Water Gain (↓ sodium concentration)*
• ↑ Insensible water loss (high fever, heatstroke, prolonged hyperventilation) • Osmotic diuretic therapy • Diarrhea	• Excessive hypotonic IV fluids • Primary polydipsia
*Disease States*	*Disease States*
• Diabetes insipidus • Primary hyperaldosteronism • Cushing syndrome • Uncontrolled diabetes mellitus	• SIADH • Heart failure • Primary hypoaldosteronism
Clinical Manifestations
*Hypernatremia With Decreased ECF Volume*	*Hyponatremia With Decreased ECF Volume*
• Restlessness, agitation, twitching, seizures, coma • Intense thirst. Dry, swollen tongue. Sticky mucous membranes • Postural hypotension, ↓ CVP, weight loss, ↑ pulse • Weakness, lethargy	• Irritability, apprehension, confusion, dizziness, personality changes, tremors, seizures, coma • Dry mucous membranes • Postural hypotension, ↓ CVP, ↓ jugular venous filling, ↑ pulse, thready pulse • Cold and clammy skin
*Hypernatremia With Normal or Increased ECF Volume*	*Hyponatremia With Normal or Increased ECF Volume*
• Restlessness, agitation, twitching, seizures, coma • Intense thirst, flushed skin • Weight gain, peripheral and pulmonary edema, ↑ BP, ↑ CVP	• Headache, apathy, confusion, muscle spasms, seizures, coma • Nausea, vomiting, diarrhea, abdominal cramps • Weight gain, ↑ BP, ↑ CVP

CVP, Central venous pressure; ECF, extracellular fluid; SIADH, syndrome of inappropriate antidiuretic hormone.

Excessive sodium intake with inadequate water intake can also lead to hypernatremia. Examples of sodium gain include IV administration of hypertonic saline or sodium bicarbonate, use of sodium-containing drugs, excessive oral intake of sodium (e.g., ingestion of seawater), and primary aldosteronism (hypersecretion of aldosterone) caused by a tumor of the adrenal glands.

Clinical Manifestations.

The manifestations of hypernatremia are primarily the result of water shifting out of cells into ECF with resultant dehydration and shrinkage of cells (see Table 17-4). Dehydration of brain cells results in neurologic manifestations such as intense thirst, agitation, and decreased alertness, ranging from sleepiness to coma.⁷ If there is any accompanying ECF volume deficit, manifestations such as postural hypotension, weakness, and decreased skin turgor occur.

Nursing and Collaborative Management Hypernatremia

Nursing Diagnoses

Nursing diagnoses and collaborative problems for the patient with hypernatremia include, but are not limited to, the following:

• Risk for injury related to altered sensorium and seizures

• Risk for fluid volume deficit related to excessive intake of sodium and/or loss of water

• Risk for electrolyte imbalance related to excessive intake of sodium and/or loss of water

• Potential complication: seizures and coma leading to irreversible brain damage

Nursing Implementation

The primary goal of treatment of hypernatremia is to treat the underlying cause. In primary water deficit, fluid replacement is provided either orally or IV with isotonic or hypotonic fluids such as 5% dextrose in water or 0.45% sodium chloride saline solution.⁸ The goal of treatment for sodium excess is to dilute the sodium concentration with sodium-free IV fluids, such as 5% dextrose in water, and to promote excretion of the excess sodium by administering diuretics. (See Chapter 50 for specific treatment of diabetes insipidus.)

Monitor serum sodium levels and the patient’s response to therapy. Quickly reducing serum sodium levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications. This risk is greatest in the patient who has developed hypernatremia over several days or longer. Dietary sodium intake is often restricted.

Hyponatremia

Hyponatremia (low serum sodium) 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 (see Table 17-4). Common causes of hyponatremia from loss of sodium-rich body fluids include profuse diaphoresis, draining wounds, excessive diarrhea or vomiting, and trauma with significant blood loss. Hyponatremia causes hypoosmolality with a shift of water into the cells.

A common cause of hyponatremia from water excess is inappropriate use of sodium-free or hypotonic IV fluids. This may occur in patients after surgery or major trauma or during administration of fluids in patients with renal failure. Patients with psychiatric disorders may have an excessive water intake. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) will result in dilutional hyponatremia caused by abnormal retention of water. (See Chapter 50 for a discussion of the causes of SIADH.)

Clinical Manifestations.

Manifestations of hyponatremia are due to cellular swelling and first manifested in the central nervous system (CNS) (see Table 17-4). The excess water lowers plasma osmolality, shifting fluid into brain cells, causing irritability, headache, confusion, seizures, and even coma. Severe acute hyponatremia, if untreated, can cause irreversible neurologic damage or death.⁷

Nursing and Collaborative Management Hyponatremia

Nursing Diagnoses

Nursing diagnoses and collaborative problems for the patient with hyponatremia include, but are not limited to, the following:

• Risk for acute confusion related to electrolyte imbalance

• Risk for injury related to altered sensorium and decreased level of consciousness

• Risk for electrolyte imbalance related to excessive loss of sodium and/or excessive intake or retention of water

• Potential complication: severe neurologic changes

Nursing Implementation

In hyponatremia caused by water excess, fluid restriction is often the only treatment. If severe symptoms (seizures) develop, small amounts of IV hypertonic saline solution (3% sodium chloride) can restore the serum sodium level while the body is returning to a normal water balance. Treatment of hyponatremia associated with abnormal fluid loss includes fluid replacement with sodium-containing solutions.

The drugs conivaptan (Vaprisol) and tolvaptan (Samsca) are given to block the activity of ADH. Conivaptan results in increased urine output without loss of electrolytes such as sodium and potassium. It should not be used in patients with hyponatremia from excess water loss. Tolvaptan is used to treat hyponatremia associated with heart failure, liver cirrhosis, and SIADH.⁹ Treatment with these drugs is started in a hospital setting so the patient’s clinical status and serum sodium levels can be carefully monitored.

Potassium Imbalances

Potassium is the major ICF cation, with 98% of the body potassium being intracellular. For example, potassium concentration within muscle cells is approximately 140 mEq/L; potassium concentration in 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. Because the ratio of ECF potassium to ICF potassium is the major factor in the resting membrane potential of nerve and muscle cells, neuromuscular and cardiac function are commonly affected by potassium imbalances.

Disruptions in the dynamic equilibrium between ICF and ECF potassium often cause clinical problems. Potassium regulates intracellular osmolality and promotes cellular growth. Potassium is required for glycogen to be deposited in muscle and liver cells. Potassium also plays a role in acid-base balance (discussed in the section on acid-base regulation later in this chapter).

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. The remainder is lost in the stool and sweat. There is an inverse relationship between sodium and potassium reabsorption in the kidneys. Factors that cause sodium retention (e.g., low blood volume, increased aldosterone level) cause potassium loss in the urine. Large urine volumes can be associated with excess loss of potassium in the urine. If kidney function is significantly impaired, retained potassium can lead to toxic levels.

Hyperkalemia

Hyperkalemia (high serum potassium) may result from impaired renal excretion, a shift of potassium from ICF to ECF, a massive intake of potassium, or a combination of these factors (Table 17-5). The most common cause of hyperkalemia is renal failure. Adrenal insufficiency with a subsequent aldosterone deficiency leads to retention of potassium ions. Factors that cause potassium to move from ICF to ECF include acidosis, massive cell destruction (as in burn or crush injury, tumor lysis, severe infections), and exercise. In metabolic acidosis, potassium ions shift from ICF to ECF in exchange for hydrogen ions moving into the cell.

TABLE 17-5

POTASSIUM IMBALANCES: CAUSES AND CLINICAL MANIFESTATIONS

Hyperkalemia (K⁺ >5.0 mEq/L [mmol/L])	Hypokalemia (K⁺ <3.5 mEq/L [mmol/L])
Causes
*Excess Potassium Intake*	*Potassium Loss*
• Excessive or rapid parenteral administration • Potassium-containing drugs (e.g., potassium penicillin) • Potassium-containing salt substitute Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Introduction Nursing Management: Sexually Transmitted Infections Nursing Management: Integumentary Problems Nursing Management: Musculoskeletal Problems Stay updated, free articles. Join our Telegram channel Tags: Medical-Surgical Nursing Assessment and Management of Clinical P Nov 17, 2016 \| Posted by admin in NURSING \| Comments Off on Fluid, Electrolyte, and Acid-Base Imbalances Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access

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