Fluid and Electrolytes Balance and Disturbance PDF

# 13 Fluid and Electrolytes: Balance and Disturbance ## Learning Objectives On completion of this chapter, the learner will be able to: 1. Differentiate between osmosis, diffusion, filtration, and active transport. 2. Describe the role of the kidneys, lungs, and endocrine glands in regulating the...

# 13 Fluid and Electrolytes: Balance and Disturbance ## Learning Objectives On completion of this chapter, the learner will be able to: 1. Differentiate between osmosis, diffusion, filtration, and active transport. 2. Describe the role of the kidneys, lungs, and endocrine glands in regulating the body's fluid composition and volume. 3. Identify the effects of aging on fluid and electrolyte regulation. 4. Plan effective care of patients with the following imbalances: fluid volume deficit and fluid volume excess, sodium deficit (hyponatremia) and sodium excess (hypernatremia), and potassium deficit (hypokalemia) and potassium excess (hyperkalemia). 5. Describe the cause, clinical manifestations, management, and nursing interventions for the following imbalances: calcium deficit (hypocalcemia) and calcium excess (hypercalcemia), magnesium deficit (hypomagnesemia) and magnesium excess (hypermagnesemia), phosphorus deficit (hypophosphatemia) and phosphorus excess (hyperphosphatemia), and chloride deficit (hypochloremia) and chloride excess (hyperchloremia). 6. Explain the roles of the lungs, kidneys, and chemical buffers in maintaining acid-base balance. 7. Compare metabolic acidosis and alkalosis with regard to causes, clinical manifestations, diagnosis, and management. 8. Compare respiratory acidosis and alkalosis with regard to causes, clinical manifestations, diagnosis, and management. 9. Interpret arterial blood gas measurements. # Glossary * **acidosis:** an acid-base imbalance characterized by an increase in H+ concentration decreased blood pH. A low arterial pH due to reduced bicarbonate concentration is called *metabolic acidosis*; a low arterial pH due to increased PCO2 is called *respiratory acidosis*. * **ascites:** a type of edema in which fluid accumulates in the peritoneal cavity. * **active transport:** physiologic pump that moves fluid from an area of lower concentration to one of higher concentration; active transport requires adenosine triphosphate for energy. * **alkalosis:** an acid-base imbalance characterized by a reduction in H+ concentration increased blood pH. A high arterial pH with increased bicarbonate concentration is called *metabolic alkalosis*; a high arterial pH due to reduced PCO2 is called *respiratory alkalosis*. * **diffusion:** the process by which solutes move from an area of higher concentration to one of lower concentration; does not require expenditure of energy. * **homeostasis:** maintenance of a constant internal equilibrium in a biologic system that involves positive and negative feedback mechanisms. * **hydrostatic pressure:** the pressure created by the weight of fluid against the wall that contains it. In the body, hydrostatic pressure in blood vessels results from the weight of fluid itself and the force resulting from cardiac contraction. * **hypertonic solution:** a solution with an osmolality higher than that of serum. * **hypotonic solution:** a solution with an osmolality lower than that of serum. * **isotonic solution:** a solution with the same osmolality as serum and other body fluids. * **osmolality:** the number of milliosmoles (the standard unit of osmotic pressure) per kilogram of solvent; expressed as *milliosmoles per kilogram* (mOsm/kg). The term *osmolality* is used more often than osmolarity to evaluate serum and urine. * **osmolarity:** the number of milliosmoles (the standard unit of osmotic pressure) per liter of solution; expressed as *milliosmoles per liter* (mOsm/L); describes the concentration of solutes or dissolved particles. * **osmosis:** the process by which fluid moves across a semipermeable membrane fr- an area of low solute concentration to an area of high solute concentration; the process continues until the solute concentrations are equal on both sides of the membrane. * **tonicity:** fluid tension or the effect that osmotic pressure of a solution with impermeable solutes exerts on cell size because of water movement across the cell membrane. # Fundamental Concepts Fluid and electrolyte balance is dependent upon dynamic processes that are crucial for life and homeostasis. Potential and actual disorders of fluid and electrolyte balance occur in every setting, with every disorder, and with a variety of changes that affect healthy people (e.g., increased fluid and sodium loss with strenuous exercise and high environmental temperature, inadequate intake of fluid and electrolytes) as well as those who are ill. ## Amount and Composition of Body Fluids Approximately 60% of a typical adult's weight consists of fluid (water and electrolytes). Factors that influence the amount of body fluid are age, gender, and body fat. In general, younger people have a higher percentage of body fluid than older adults, and men have proportionately more body fluid than women. People who are obese have less fluid than those who are thin, because fat cells contain little water. The skeleton also has low water content. Muscle, skin, and blood contain the highest amounts of water. Body fluid is located in two fluid compartments: the intracellular space (fluid in the cells) and the extracellular space (fluid outside the cells). Approximately two thirds of body fluid is in the intracellular fluid (ICF) compartment and is located primarily in the skeletal muscle mass. Approximately one third is in the extracellular fluid (ECF) compartment. The ECF compartment is further divided into the intravascular, interstitial, and transcellular fluid spaces: * The intravascular space (the fluid within the blood vessels) contains plasma, the effective circulating volume. Approximately 3 L of the average 6 L of blood volume in adults is made up of plasma. The remaining 3 L is made up of erythrocytes, leukocytes, and thrombocytes. * The interstitial space contains the fluid that surrounds the cell and totals about 11 to 12 L in an adult. Lymph is an interstitial fluid. * The transcellular space is the smallest division of the ECF compartment and contains approximately 1 L. Examples of transcellular fluids include cerebrospinal, pericardial, synovial, intraocular, and pleural fluids, sweat, and digestive secretions. ## Osmosis and Osmolality When two different solutions are separated by a membrane that is impermeable to the dissolved substances, fluid shifts through the membrane from the region of low solute concentration to the region of high solute concentration until the solutions are of equal concentration. This diffusion of water caused by a fluid concentration gradient is known as osmosis. The magnitude of this force depends on the number of particles dissolved in the solutions, not on their weights. The number of dissolved particles contained in a unit of fluid determines the osmolality of a solution, which influences the movement of fluid between the fluid compartments. Tonicity is the ability of all solutes to cause an osmotic driving force that promotes water movement from one compartment to another. The control of tonicity determines the normal state of cellular hydration and cell size. Sodium, mannitol, glucose, and sorbitol are effective osmoles (capable of affecting water movement). Three other terms are associated with osmosis - osmotic pressure, oncotic pressure, and osmotic diuresis: * Osmotic pressure is the amount of hydrostatic pressure needed to stop the flow of water by osmosis. It is primarily determined by the concentration of solutes. Oncotic pressure is the osmotic pressure exerted by proteins (e.g., albumin). Osmotic diuresis is the increase in urine output caused by the excretion of substances, such as glucose, mannitol, or contrast agents in the urine. ## Diffusion Diffusion is the natural tendency of a substance to move from an area of higher concentration to one of lower concentration. It occurs through the random movement of ions and molecules. Examples of diffusion are the exchange of oxygen and carbon dioxide between the pulmonary capillaries and alveoli and the tendency of sodium to move from the ECF compartment, where the sodium concentration is high, to the ICF, where its concentration is low. ## Filtration Hydrostatic pressure in the capillaries tends to filter fluid out of the intravascular compartment into the interstitial fluid. Movement of water and solutes occurs from an area of high hydrostatic pressure to an area- low hydrostatic pressure. The kidneys filter approximately 180 L of plasma per day. Another example of filtration is the passage of water and electrolytes from the arterial capillary bed to- interstitial fluid; in this instance, the hydrostatic pressure results from the pumping action of the heart. ## Sodium-Potassium Pump The sodium concentration is greater in the ECF than in the ICF; because of this, sodium tends to enter the cell by diffusion. This tendency is offset by the sodium-potassium pump that is maintained by the cell membrane and actively moves sodium from the cell into the ECF. Conversely, the high intracellular potassium concentration is maintained by pumping potassium into the cell. By definition, active transport implies that energy must be expended for the movement to occur against a concentration gradient. ## Systemic Routes of Gains and Losses Water and electrolytes are gained in various ways. Healthy people gain fluids by drinking and eating, and their daily average I&O of water are approximately equal. ## Kidneys The usual daily urine volume in the adult is 1 to 2 L. A general rule i- that the output is approximately 1 mL of urine per kilogram of body weight per hour in all age groups. ## Skin Sensible perspiration refers to visible water and electrolyte loss through the skin (sweating). The chief solutes in sweat are sodium, chloride, and potassium. Actual sweat losses can vary from 0 to 1000 mL or more every hour, depending on factors such as the environmental temperature. Continuous water loss by evaporation (approximately 500 mL/day) occurs through the skin as insensible perspiration, a nonvisible form of water loss. Fever and exercise greatly increase insensible water loss through the skin and the lungs and the skin, as does the loss of the natural skin barrier (e.g., through major burns). ## Lungs The lungs normally eliminate water vapor (insensible loss) at a rate of approximately 300 mL every day. The loss is much greater with increased respiratory rate or depth, or in a dry climate. ## Gastrointestinal Tract The usual loss through the gastrointestinal (GI) tract is 100 to 200 mL daily, even though approximately 8 L of fluid circulates through the GI system every 24 hours. Because the bulk of fluid is normally reabsorbed in the small intestine, diarrhea and fistulas cause large losses. ## Laboratory Tests for Evaluating Fluid Status **Osmolality** is the concentration of fluid that affects the movement of water between fluid compartments by osmosis. Osmolality measures the solute concentration per kilogram in blood and urine. It is also a measure of a solution's ability to create osmotic pressure and affect the movement of water. Serum osmolality primarily reflects the concentration of sodium, although blood urea nitrogen (BUN) and glucose also play a major role in determining serum osmolality. Urine osmolality is determined by urea, creatinine, and uric acid. When measured with serum osmolality, urine osmolality is the most reliable indicator of urine concentration. Osmolality is reported as milliosmoles per kilogram of water (mOsm/kg). In healthy adults, normal serum osmolality is 275 to 290 mOsm/kg. Sodium predominates in ECF osmolality and holds water in this compartment. Factors that increase and decrease serum and urine osmolality are identified in the table below. Serum osmolality may be measured directly through laboratory tests or estimated at the bedside by doubling the serum sodium level or by using the following formula: ``` Na+ x 2 = Glucose BUN + 18 3 = Approximate value of serum osmolality ``` **Osmolarity**, another term that describes the concentration of solutions, is measured in milliosmoles per liter (mOsm/L). However, the term *osmolality* is used more often in clinical practice. The value of osmolarity is usually within 10 mOsm of the value of osmolality. | Fluid | Factors Increasing Osmolality | Factors Decreasing Osmolality | |:---|:---|:---| | Serum (275-290 mOsm/kg water) | Severe dehydration, Free water loss, Diabetes insipidus, Hypernatremia, Hyperglycemia, Stroke or head injury, Renal tubular necrosis, Consumption of methanol or ethylene glycol (antifreeze), High anion gap metabolic acidosis, Mannitol therapy | Fluid volume excess, Syndrome of inappropriate antidiuretic hormone (SIADH), Acute kidney injury, Diuretic use, Adrenal insufficiency, Hyponatremia, Overhydration, Paraneoplastic syndrome associated with lung cancer, Advanced severe liver disease, Alcoholism | | Urine (50-800 mOsm/kg water) | Fluid volume deficit, SIADH, Congestive heart failure, Acidosis, Prerenal failure | Fluid volume excess, Diabetes insipidus, Hyponatremia, Aldosteronism, Pyelonephritis, Acute tubular necrosis | **Urine-specific gravity** measures the kidneys' ability to excrete or conserve water. The specific gravity of urine is compared- the weight of distilled water, which has a specific gravity of 1.000. The normal range of urine specific gravity is 1.010 to 1.025. Urine specific gravity can be measured by sending approximately 20 mL of urine to the laboratory testing, or carefully assessed with dipstick. Specific gravity varies inversely with urine volume; normally, the larger the volume of urine, the lower the specific gravity is. Specific gravity i- less reliable indicator of concentration than urine osmolality; increased glucose or protein in urine can cause a falsely elevated specific gravity. Factors that increase or decrease urine osmolality are the same as those for urine specific gravity. **BUN** is made up of urea, which is an end product of the metabolism of protein from both muscle and dietary intake by the liver. Amino acid breakdown produces large amounts of ammonia molecules, which are absorbed into the bloodstream. Ammonia molecules are converted to urea and excreted in the urine. The normal BUN is 10 to 20 mg/dL (3.6 to 7.2 mmol/L). The BUN level varies with urine output. Factors that increase BUN include decreased renal function, GI bleeding, dehydration, increased protein intake, fever, and sepsis. Those that decrease BUN include end-stage liver disease, a low-protein diet, starvation, and any condition that results in expanded fluid volume (e.g., pregnancy). **Creatinine** is the end product of muscle metabolism. It is a better indicator of renal function than BUN because it does not vary with protein intake and metabolic state. The normal serum creatinine is approximately 0.7 to 1.4 mg/dL (62 to 124 mmol/L); however, its concentration depends on lean body mass and varies from person to person. Serum creatinine levels increase when renal function decreases. **Hematocrit** measures the volume percentage of red blood cells (erythrocytes) in whole blood and normally ranges from 42% to 52% for men and 35% to 47% for women. Conditions that increase the hematocrit value are dehydration and polycythemia, and those that decrease hematocrit are overhydration anemia. **Urine sodium values** change with sodium intake and the status of fluid volume: As sodium intake increases, excretion increases; as the circulating fluid volume decreases, sodium is conserved. Normal urine sodium levels range from 75 to 200 mEq/24 hours (75 to 200 mmol/24 hours). A random specimen usually contains more than 40 mEq/L of sodium. Urine sodium levels are used to assess volume status and are useful in the diagnosis of hyponatremia and acute kidney injury. ## Homeostatic Mechanisms The body is equipped with remarkable homeostatic mechanisms to keep the composition and volume of body fluid within narrow limits of normal. Organs involved in homeostasis include the kidneys, heart, lungs, pituitary gland, adrenal glands, and parathyroid glands. ## Kidney Functions Vital to the regulation of fluid and electrolyte balance, the kidneys normally filter 180 L of plasma every day in the adult and excrete 1 to 2 L of urine. They act both autonomously and in response to bloodborne messengers, such as aldosterone and antidiuretic hormone (ADH). Major functions of the kidneys in maintaining normal fluid balance include the following: * Regulation of ECF volume and osmolality by selective retention and excretion of body fluids. * Regulation of normal electrolyte levels in the ECF by selective electrolyte retention and excretion. * Regulation of pH of the ECF by retention of hydrogen ions. * Excretion of metabolic wastes and toxic substances. Given these functions, failure of the kidneys results in multiple fluid and electrolyte abnormalities. ## Heart and Blood Vessel Functions The pumping action of the heart circulates blood through the kidneys under sufficient pressure to allow for urine formation. Failure of this pumping action interferes with renal perfusion and thus with water and electrolyte regulation. ## Lung Functions The lungs are also vital in maintaining homeostasis. Through exhalation, the lungs remove approximately 300 mL of water daily in the normal adult. Abnormal conditions, such as hyperpnea (abnormally deep respiration) or continuous coughing, increase this loss; mechanical ventilation with excessive moisture decreases it. The lungs also play a major role in maintaining acid-base balance. ## Pituitary Functions The hypothalamus manufactures ADH, which is stored in the posterior pituitary gland and released as needed to conserve water. Functions of ADH include maintaining the osmotic pressure of the cells by controlling the retention or excretion of water by the kidneys and by regulating blood volume. ## Adrenal Functions Aldosterone, a mineralocorticoid secreted by the zona glomerulosa (outer zone) of the adrenal cortex, has a profound effect on fluid balance. Increased secretion of aldosterone causes sodium retention (and thus water retention) and potassium loss. Conversely, decreased secretion of aldosterone causes sodium and water loss and potassium retention. Cortisol, another adrenocortical hormone, has less mineralocorticoid action. However, when secreted in large quantities (or given as corticosteroid therapy), it can also produce sodium and fluid retention. ## Parathyroid Functions The parathyroid glands, embedded in the thyroid gland, regulate calcium and phosphate balance by means of parathyroid hormone (PTH). PTH influences bone reabsorption, calcium absorption from the intestines, and calcium reabsorption from the renal tubules.. ## Other Mechanisms Changes in the volume of the interstitial compartment within the ECF can occur without affecting body function. However, the vascular compartment cannot tolerate change as readily and must be carefully maintained to ensure that tissues receive adequate nutrients. ## Baroreceptors The baroreceptors are located in the left atrium and the carotid and aortic arches. These receptors respond to changes in the circulating blood volume and regulate sympathetic and parasympathetic neural activity as well as endocrine activities. As arterial pressure decreases, baroreceptors transmit fewer impulses from the carotid and the aortic arches to the vasomotor center. A decrease in impulses stimulates the sympathetic nervous system and inhibits the parasympathetic nervous system. The outcome is an increase in cardiac rate, conduction, and contractility and an increase in circulating blood volume. Sympathetic stimulation constricts renal arterioles; this increases the release of aldosterone, decreases glomerular filtration, and increases sodium and water reabsorption. ## Renin-Angiotensin-Aldosterone System Renin is an enzyme that converts angiotensinogen, a substance formed by the liver, into angiotensin I. Renin is released by the juxtaglomerular cells of the kidneys in response to decreased renal perfusion. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II, with its vasoconstrictor properties, increases arterial perfusion pressure and stimulates thirst. As the sympathetic nervous system is stimulated, aldosterone is released in response to an increased release of renin. Aldosterone is a volume regulator and is also released as serum potassium increases, serum sodium decreases, or adrenocorticotropic hormone (ACTH) increases. ## Antidiuretic Hormone and Thirst ADH and the thirst mechanism have important roles in maintaining sodium concentration and oral intake of fluids. Oral intake is controlled by the thirst center located in the hypothalamus. As serum concentration or osmolality increases or blood volume decreases, neurons in the hypothalamus are stimulated by intracellular dehydration; thirst then occurs, and the person increases their intake of oral fluids. Water excretion is controlled- ADH, aldosterone, and baroreceptors. The presence or absence of ADH is the most significant factor in determining whether the urine that is excreted is concentrated or dilute. ## Osmoreceptors Located on - surface of the hypothalamus, osmoreceptors sense changes in sodium concentration. As osmotic pressure increases, the neurons become dehydrated and quickly release impulses to the posterior pituitary, which increases the release of ADH, which then travels in the blood to the kidneys, where it alters permeability to water, causing increased reabsorption of water and decreased urine output. The retained water dilutes the ECF and returns its concentration to normal. Restoration of normal osmotic pressure provides feedback to the osmoreceptors to inhibit further ADH release. ## Natriuretic Peptides Natriuretic peptide hormones affect fluid volume and cardiovascular function through the excretion of sodium (natriuresis), direct vasodilation, and opposition of the rennin-angiotensin-aldosterone system. Four peptides have been identified. The first is atrial natriuretic peptide (ANP) produced by the atrial myocardium with tissue distribution in the cardiac atria and ventricles. The second is brain natriuretic peptide (BNP) produced by the ventricular myocardium with tissue distribution in the brain and cardiac ventricles. ANP, also called atrial natriuretic factor, atrial natriuretic hormone, or atriopeptin, is a peptide that is synthesized, stored, and released by muscle cells of the atria of the heart in response to several factors. These factors include increased atrial pressure, angiotensin II stimulation, endothelin (a powerful vasoconstrictor of vascular smooth muscle that is a peptide released from damaged endothelial cells in the kidneys or other tissues), and sympathetic stimulation. Any condition that results in volume expansion (exercise, pregnancy), calorie restriction, hypoxia, or increased cardiac filling pressures (e.g., high sodium intake, heart failure, chronic kidney disease, atrial tachycardia, or use of vasoconstrictor agents such as epinephrine) increases release of ANP and BNP. ANP's action decreases water, sodium, and adipose loads on the circulatory system to decrease blood pressure. The action of ANP is therefore directly opposite of the renin-angiotensin-aldosterone system. The ANP measured in plasma is normally 20 to 77 pg/mL (20 to 77 ng/L). This level increases in acute heart failure, paroxysmal supraventricular tachycardia, hyperthyroidism, subarachnoid hemorrhage, and small cell lung cancer. The level decreases in chronic heart failure and with the use of medications such as enalapril. The third peptide is C-type natriuretic peptide (CNP), which has tissue distribution in the brain, ovary, uterus, testis, and epididymis. The fourth peptide is D-type natriuretic peptide (DNP) -- newest peptide with structural similarities to ANP, BNP, and CNP. # Gerontologic Considerations Normal physiologic changes of aging, including reduced cardiac, renal, and respiratory function and reserve and alterations in the ratio of body fluids to muscle mass, may alter older adults' responses to fluid and electrolyte changes and acid-base disturbances. Decreased respiratory function can cause impaired pH regulation in older adults with major illness or trauma. Renal function declines with age, as do muscle mass and daily exogenous creatinine production. Therefore, high-normal and minimally elevated serum creatinine values may indicate substantially reduced renal function in older adults. Because of a decrease in age-related muscle mass, older adults have a lower concentration of body fluid that may alter physiologic responses. # Fluid Volume Disturbances ## Hypovolemia FVD, or hypovolemia, occurs when loss of ECF volume exceeds the intake of fluid. It occurs when water and electrolytes are lost in the same proportion as they exist in normal body fluids; thus, the ratio- serum electrolytes to- water remains the same. FVD should not be confused with dehydration, which refers to loss of water alone, with increased serum sodium levels. FVD may occur alone or in combination with other imbalances. Unless other imbalances are present concurrently, serum electrolyte concentrations remain essentially unchanged. ### Pathophysiology FVD results from loss of body fluids and occurs more rapidly when coupled with decreased fluid intake. FVD can also develop with a prolonged period of inadequate intake. Causes of FVD include abnormal fluid losses, such as those resulting from vomiting, diarrhea, GI suctioning, and sweating; decreased intake, as in nausea or lack of access to fluids; and third-space fluid shifts, or the movement of fluid from the vascular system to other body spaces (e.g., with edema formation in burns, ascites with liver dysfunction). Additional causes include diabetes insipidus (a decreased ability to concentrate urine owing to a defect in the kidney tubules that interferes with water reabsorption), adrenal insufficiency, osmotic diuresis, hemorrhage, and coma. | Imbalance | Contributing Factors | Signs/Symptoms and Laboratory Findings | |---|---|---| | Fluid volume deficit (hypovolemia) | Lose of water and electrolytes, as in vomiting, diarrhea, fistulas, fever, excess sweating, burns, blood loss, gastrointestinal suction, and third-space fluid shifts; and decreased intake, as in anorexia, canes, and inability to gain access to fluid. Diabetes insipidus and uremia both contribute to a depletion of extracellular fluid volume. | Acute weight loss, skin turgor, oliguria, concentrated urine, capillary refilling time prolonged, low CVP, flattened neck veins, dizziness, weakness, thirst, and confusion, rapid pulse, muscle cramps, sunken eyes, nausea, increased temperature, cool, clammy, pale skin. Labs indicate: ↓ hemoglobin and hematocrit, ↑ serum and urine osmolality and specific gravity, ↑ urine sodium, ↑ BUN and creatinine, ↑ urine specific gravity and osmolality. | | Fluid volume excess (hypervolemia) | Compromised regulatory mechanisms, such as kidney injury, heart failure, and cirrhosis; overzealous administration of sodium-containing fluids and fluid shifts (e.g., treatment- burns). Prolonged corticosteroid therapy, severe stress, and hyperalbuminemia augment fluid volume excess. | Acute weight gain, peripheral edema and ascites, distended jugular veins, crackles, elevated CVP, shortness of breath, ↑ BP, bounding pulse and cough, ↑ respiratory rate, ↓ urine output. Labs indicate: ↓ hemoglobin and hematocrit, ↑ serum and urine osmolality, ↑ urine sodium and specific gravity. | ### Clinical Manifestations FVD can develop rapidly, and its severity depends on the degree of fluid loss. Clinical signs and symptoms and laboratory findings are presented in the table below. | Assessment and Diagnostic Findings | |---|---| | Laboratory data useful in evaluating fluid volume status include BUN and its relation to serum creatinine concentration. Normal BUN to serum creatinine concentration ratio is 10:1. A volume-depleted patient has a BUN elevated out of proportion to the serum creatinine (ratio greater than 20:1). | The presence and cause of hypovolemia may- determined through the health history and physical examination. In addition, the hematocrit level is greater than normal because there is a decreased plasma volume. | Serum electrolyte changes may also exist. Potassium and sodium levels can be reduced (hypokalemia, hyponatremia) or elevated (hyperkalemia, hypernatremia). * Hypokalemia occurs with GI and renal losses. * Hyperkalemia occurs with adrenal insufficiency. * Hyponatremia occurs with increased thirst and ADH release. * Hypernatremia results from increased insensible losses and diabetes insipidus. | There may or may not- a decrease in urine (oliguria) in hypovalemia. Urine specific gravity is increased in relation to the kidneys' attempt to conserve water and is decreased with diabetes insipidus. Aldosterone i- secreted when fluid volume is low causing reabsorption of sodium and chloride, resulting in decreased urinary sodium and chloride. Urine osmolality can be greater than 450 mOsm/kg because the kidneys try to compensate by conserving water. ## Hypervolemia Fluid volume excess (FVE), or hypervolemia, refers to an isotonic expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ECF. It is most often secondary to an increase in the total-body sodium content, which, in turn, leads to an increase in total-body water. Because there is isotonic retention of body substances, the serum sodium concentration remains essentially normal. ### Pathophysiology FVE may- related to simple fluid overload or diminished function of the homeostatic mechanisms responsible for regulating fluid balance. Contributing factors can include heart failure, kidney injury, and cirrhosis of the liver. Another contributing factor is consumption of excessive amounts of table or other sodium salts. Excessive administration of sodium-containing fluids in a patient with impaired regulatory mechanisms may predispose him or her to a serious FVE as well. ### Clinical Manifestations Clinical manifestations of FVE result from expansion of the ECF and may include edema, distended neck veins, and crackles (abnormal lung sounds). Further discussion of clinical signs and symptoms and laboratory findings can be found in the table below. | Assessment and Diagnostic Findings | |---|---| | Laboratory data useful in diagnosing FVE include BUN and hematocrit levels. In FVE, both of these values may be decreased because- plasma dilution, low protein intake, and anemia. In chronic kidney disease, both serum osmolality and the sodium level are decreased owing to excessive retention of water. The urine sodium level is increased if the kidneys are attempting to excrete excess volume. A chest x-ray may reveal pulmonary congestion. Hypervolemia occurs when aldosterone is chronically stimulated (i.e., cirrhosis, heart failure, and nephrotic syndrome). Therefore, the urine sodium level does not increase in these conditions. | ### Medical Management Management of FVE is directed at the causes, and if related to excessive administration of sodium-containing fluids, discontinuing the infusion may be all that is needed. Symptomatic treatment consists of administering diuretics and restricting fluids and sodium. ### Pharmacologic Therapy Diuretics are prescribed when dietary restriction of sodium alone i- insufficient to reduce edema by inhibiting the reabsorption of sodium and water by the kidneys. The choice of diuretic is based on the severity of the hypervolemic state, the degree of impairment of renal function, and the potency of the diuretic. Thiazide diuretics block sodium reabsorption in the distal tubule, where only 5% to 10% of filtered sodium is reabsorbed. Loop diuretics, such as furosemide (Lasix) or torsemide (Demadex), can cause a greater loss of both sodium and water because they block sodium reabsorption in the ascending limb of Henle loop, where 20% to 30% of filtered sodium is normally reabsorbed. Generally, thiazide diuretics, such as hydrochlorothiazide (Microzide), are prescribed for mild to moderate hypervolemia and loop diuretics for severe hypervolemia. Electrolyte imbalances may result from side effects of diuretics. Hypokalemia can occur with all diuretics except those that work in the last distal tubule of the nephrons. Potassium supplements can be prescribed to avoid this complication. Hyperkalemia can occur with diuretics that work in the distal tubule (e.g., spironolactone [Aldactone], a potassium-sparing diuretic), especially in patients with decreased renal function. Hyponatremia occurs with diuresis owing to increased release of ADH secondary to reduction in circulating volume. Decreased magnesium levels occur with administration of loop and thiazide diuretics due to decreased reabsorption and increased excretion of magnesium by the kidney. Azotemia (increased nitrogen levels in the blood) can occur with FVE when urea and creatinine are not excreted owing to decreased perfusion by the kidneys and decreased excretion of wastes. High uric acid levels (hyperuricemia) can also occur from increased reabsorption and decreased excretion of uric acid by the kidneys. ### Dialysis If renal function i- so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium- fluid from the body. Hemodialysis or peritoneal dialysis may be used to remove nitrogenous wastes and control potassium and acid-base balance, and to remove sodium and fluid. Continuous renal replacement therapy may also be required. ### Nutritional Therapy Treatment of FVE usually involves dietary restriction of sodium. An average daily diet not restricted in sodium contains 6 to 15 g of salt, whereas low-sodium diets can range from a mild restriction- as little as 250 mg of sodium per day, depending on the patient's- For a mild sodium-restricted diet allow oly light salting of food (about half the usual amount) in cooking and at the table, and no addition of salt to commercials prepared foods that are already seasoned. Foods high in sodium must e avoided. It is the sodium salt (sodium chloride) rather than sodium itself that contributes- edema. Therefore, patients are instructed to read food labels carefully to determine salt content. Because about half of ingested sodium is in the form of seasoning, seasoning substitutes can play a major role in decreasing sodium intake. Lemon juice, onions, and garlic are excellent substitute flavorings, although some patients prefer salt substitutes. Most salt substitutes contain potassium and must therefore be use cautiously by patients taking potassium-sparing diuretics (e.g., spironolactone, triamterene, amiloride). They should not- used in conditions associated with potassium retention, such as advanced renal disease. Salt substitutes containing ammonium chloride can- harmful to patients with liver damage. In some communities, drinking water mat contain too much sodium for a sodium-restricted diet. Depending on its source, water may contain as little as 1 mg or more than 1500 mg of sodium per quart. Patients may need to use distilled water if the local water supply is very high in sodium. Bottled water can have a sodium content that ranges from 0 to 1200 mg/L; therefore, if sodium is restricted, the label must- carefully examined for sodium content before purchasing and drinking bottled water. Also. patients on sodium-restricted diets should- cautioned to avoid water softeners that add sodium to water in exchange for other ions, such as calcium. Protein intake may be increased in patients who are malnourished or who have low serum protein levels in an effort to increase capillary oncotic pressure and pull fluid out of the tissues into vessels for excretion by the kidneys. ### Nursing Management To assess for FVE, the nurse measures I&O at regular intervals to identify excessive fluid retention. The patient is weighed daily, and rapid weight gain is noted. An acute weight gain of 1 kg (2.2 lb) is equivalent to a gain of approximately 1 L of fluid. Breath sounds are assessed at regular intervals in at-risk patients, particularly if parenteral fluids are being given. The nurse monitors the degree of edema in the most dependent parts of the body, such as the feet and ankles in ambulatory patients and the sacral region in patients confined to bed. Pitting edema is assessed by pressing a finger into the affected part, creating a pit or indentation that is evaluated on a scale of 1+ (minima) to 4+ (severe). Peripheral edema is monitored by measuring the circumference of the extremity with a tape marked in millimeters. ### Preventing Hypervolemia Specific interventions vary with the underlying condition and the degree of FVE. However, most patients require sodium-restricted diets in some form, and adherence to the prescribed diet- encouraged. Patients are instructed to avoid over-the-counter (OTC) medications without first checking with a health care provider, because they may contain sodium (e.g., Alka-Seltzer). If fluid retention persists despite adherence to a prescribed diet, hidden sources of sodium, such as the water supply or use of water softeners, should be considered. ## Detecting and Controlling Hypervolemia It is important to detect FVE before the condition becomes severe. Interventions include promoting rest, restricting sodium intake, monitoring parenteral fluid therapy, and administering appropriate medications. Regular rest periods may be beneficial, because bed rest favors diuresis of fluid. The mechanism is related to diminished venous pooling and the subsequent increase in effective circulating blood volume and renal perfusion. Sodium and fluid restriction should be instituted as indicated. Because most patients with FVE require diuretics, the patient's response to these agents is monitored. The rate of parenteral fluids and the patient's response to these fluids are also closely monitored. If dyspnea or orthopnea is present, the patient is placed in a semi-Fowler position to promote lung expansion. The patient is turned and repositioned at regalar intervals because edematous tissue is more prone to skin breakdown than normal tissue. Because conditions predisposing to FVE are likely to be chronic, patients are taught- monitor their response to therapy by documenting fluid I&O and body weight changes. The importance of adhering to the treatment regimen is emphasized. ## Educating Patients About Edema Because edema is a common manifestation of FVE, patients need to recognize its symptoms and understand its importance. The nurse gives special attention to edema when instructing the patient with FVE. Edema can occur as a result of increased capillary fluid pressure, decreased capillary oncotic pressure, or increased interstitial oncotic pressure, causing expansion of the interstitial fluid compartment. Edema can be localized (e.g., in the ankle, as in rheumatoid arthritis) or generalized (as cardiac failure and kidney injury). Severe generalized edema is called *anasarca*. Edema occurs when there is a change in the capillary membrane, increasing the formation of interstitial fluid or decreasing the removal of interstitial fluid. Sodium retention is a frequent cause of the increased ECF volume. Burns and infection are- examples of conditions associated with increased interstitial fluid volume. Obstructions to lymphatic outflow, a plasma albumin level less than 1.5 to 2 g/dL, or a decrease in plasma oncotic pressure contributes to increased interstitial fluid volume. The kidneys retain sodium and water when there is decreased ECF volume as a result of decreased carcia- output from heart failure. A thorough medication history is necessary to identify any medications that could cause edema, such as nonsteroidal anti-inflammatory drugs (NSAIDs), estrogens, corticosteroids, and