Fluid and Electrolytes PDF
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This document provides a detailed analysis of fluid and electrolyte balance in the human body. It explains the physiology of these crucial substances along with the role of various organs in maintaining homeostasis. It also discusses different types of fluid and electrolytes, their concentration, movements, and imbalances, affecting the body's equilibrium.
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Fundamental Concepts Nurses need to understand the physiology of fluid and electrolyte balance and acid–base balance to anticipate, identify, and respond to possible imbalances. Nurses use effective education and communication skills to help prevent and treat various fluid and electrolyte disturbanc...
Fundamental Concepts Nurses need to understand the physiology of fluid and electrolyte balance and acid–base balance to anticipate, identify, and respond to possible imbalances. Nurses use effective education and communication skills to help prevent and treat various fluid and electrolyte disturbances. Amount and Composition of Body Fluids Approximately 60% of a typical adult’s weight consists of fluid (water and electrolytes) (see Fig. 13-1). 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 (Grossman & Porth, 2014). 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 (Grossman & Porth, 2014). 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. The ECF transports electrolytes; it also carries other substances, such as enzymes and hormones. Body fluid normally moves between the two major compartments or spaces in an effort to maintain equilibrium between the spaces. Loss of fluid from the body can disrupt this equilibrium. Sometimes fluid is not lost from the body but is unavailable for use by either the ICF or ECF. Loss of ECF into a space that does not contribute to equilibrium between the ICF and the ECF is referred to as a third-space fluid shift, or third spacing (Papadakis & McPhee, 2016). Early evidence of a third-space fluid shift is a decrease in urine output despite adequate fluid intake. Urine output decreases because fluid shifts out of the intravascular space; the kidneys then receive less blood and attempt Medical Surgical Nursing Fluids & Electrolytes to compensate by decreasing urine output. Other signs and symptoms of third spacing that indicate an intravascular fluid volume deficit (FVD) include increased heart rate, decreased blood pressure, decreased central venous pressure, edema, increased body weight, and imbalances in fluid intake and output (I&O). This fluid will be reabsorbed back into the extracellular space over a period of a few days to a few weeks. However, the acute volume depletion must be restored to prevent further complications. Examples of causes of third-space fluid losses include intestinal obstruction, pancreatitis, crushing traumatic injuries, bleeding (trauma or dissected aortic aneurysm), peritonitis, and major venous obstruction (Sterns, 2014a) Electrolytes Electrolytes in body fluids are active chemicals (cations that carry positive charges and anions that carry negative charges). The major cations in body fluid are sodium, potassium, calcium, magnesium, and hydrogen ions. The major anions are chloride, bicarbonate, phosphate, sulfate, and proteinate ions. These chemicals unite in varying combinations. Therefore, electrolyte concentration in the body is expressed in terms of milliequivalents (mEq) per liter, a measure of chemical activity, rather than in terms of milligrams (mg), a unit of weight. More specifically, a milliequivalent is defined as being equivalent to the electrochemical activity of 1 mg of hydrogen. In a solution, cations and anions are equal in milliequivalents per liter. Electrolyte concentrations in the ICF differ from those in the ECF. Because special techniques are required to measure electrolyte concentrations in the ICF, it is customary to measure the electrolytes in the most accessible portion of the ECF—namely, the plasma. Sodium ions, which are positively charged, far outnumber the other cations in the ECF. Because sodium concentration affects the overall concentration of the ECF, sodium is important in regulating the volume of body fluid. Retention of sodium is associated with fluid retention, and excessive loss of sodium is usually associated with decreased volume of body fluid. The major electrolytes in the ICF are potassium and phosphate. The ECF has a low concentration of potassium and can tolerate only small changes in potassium concentrations. Therefore, the release of large stores of intracellular potassium, typically caused by trauma to the cells and tissues, can be extremely dangerous. Medical Surgical Nursing Fluids & Electrolytes The body expends a great deal of energy maintaining the high extracellular concentration of sodium and the high intracellular concentration of potassium. It does so by means of cell membrane pumps that exchange sodium and potassium ions. Normal movement of fluids through the capillary wall into the tissues depends on hydrostatic pressure (the pressure exerted by the fluid on the walls of the blood vessel) at both the arterial and the venous ends of the vessel and the osmotic pressure exerted by the protein of plasma. The direction of fluid movement depends on the differences in these two opposing forces (hydrostatic vs. osmotic pressure). Regulation of Body Fluid Compartments 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 (see Fig. 13-2A). 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 (see Fig. 13-2B). It occurs through the random movement of ions and molecules (Grossman & Porth, 2014). Examples of diffusion are the exchange of oxygen and carbon dioxide (CO2) 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. Medical Surgical Nursing Fluids & Electrolytes 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 of 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 the 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 (Grossman & Porth, 2014; Sterns, 2014a). A general rule is that the output is approximately 1 mL of urine per kilogram of body weight per hour (1 mL/kg/h) 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 (Grossman & Porth, 2014). Fever and exercise greatly increase insensible water loss through the lungs and the skin, as does the loss of the natural skin barrier (e.g., through major burns) (Earhart, Weiss, Rahman, et al., 2015; Sterns, 2014b). Lungs The lungs normally eliminate water vapor (insensible loss) at a rate of approximately 300 mL every day (Grossman & Porth, 2014). 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. Medical Surgical Nursing Fluids & Electrolytes 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 (Grossman & Porth, 2014). 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 (Inker & Perrone, 2014). They act both autonomously and in response to bloodborne messengers, such as aldosterone and antidiuretic hormone (ADH) (Grossman & Porth, 2014). 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 (Inker & Perrone, 2014) 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 (Sterns, 2014d). 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 Medical Surgical Nursing Fluids & Electrolytes 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 (Hall, 2015). Renin–Angiotensin–Aldosterone System Renin is an enzyme that converts angiotensinogen, a substance formed by the liver, into angiotensin I (Grossman & Porth, 2014). Renin is released by the juxtaglomerular cells of the kidneys in response to decreased renal perfusion (McGloin, 2015). 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 (Sterns, 2014e). Oral intake is controlled by the thirst center located in the hypothalamus (Grossman & Porth, 2014). 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 by ADH, aldosterone, and baroreceptors, as mentioned previously. 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 the surface of the hypothalamus, osmoreceptors sense changes in sodium concentration. As osmotic pressure increases, the neurons become Medical Surgical Nursing Fluids & Electrolytes 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 the 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 (Colucci & Chen, 2014). 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 the 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 (Vasotec) (Frandsen & Pennington, 2014). 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)—the newest peptide with structural similarities to ANP, BNP, and CNP. 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 of 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. Medical Surgical Nursing Fluids & Electrolytes Clinical Manifestations FVD can develop rapidly, and its severity depends on the degree of fluid loss. 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) (Sterns, 2014a). The presence and cause of hypovolemia may be 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 be 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 is 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. Medical Management When planning the correction of fluid loss for the patient with FVD, the primary provider considers the patient’s maintenance requirements and other factors (e.g., fever) that can influence fluid needs. If the deficit is not severe, the oral route is preferred, provided the patient can drink. However, if fluid losses are acute or severe, the IV route is required. Isotonic electrolyte solutions (e.g., lactated Ringer solution, 0.9% sodium chloride) are frequently the first-line choice to treat the hypotensive patient with FVD because they expand plasma volume (Sterns, 2014e). As soon as the patient becomes normotensive, a hypotonic electrolyte solution (e.g., 0.45% sodium chloride) is often used to provide both electrolytes and water for renal excretion of metabolic wastes. Accurate and frequent assessments of I&O, weight, vital signs, central venous pressure, level of consciousness, breath sounds, and skin color are monitored to determine when therapy should be slowed to avoid volume overload. The rate of fluid administration is based on the severity of loss and the patient’s hemodynamic response to volume replacement. If the patient with severe FVD is not excreting enough urine and is therefore oliguric, the primary provider needs to determine whether the depressed renal function is caused by reduced renal blood flow secondary to FVD (prerenal azotemia) or, more seriously, by acute tubular necrosis from prolonged FVD. The test used in this situation is referred to as a fluid challenge test. During a fluid challenge test, volumes of fluid are given at specific rates and intervals while the patient’s hemodynamic response to this treatment is monitored (i.e., vital signs, breath sounds, orientation status, central venous pressure, urine output). Medical Surgical Nursing Fluids & Electrolytes Shock can occur when the volume of fluid lost exceeds 25% of the intravascular volume or when fluid loss is rapid. Nursing Management To assess for FVD, the nurse monitors and measures fluid I&O at least every 8 hours, and sometimes hourly. Researchers have reported that maintaining an accurate I&O is a particular challenge with patients in critical care settings (Diacon & Bell, 2014) (see Chart 13-1). As FVD develops, body fluid losses exceed fluid intake through excessive urination (polyuria), diarrhea, vomiting, or other mechanisms. Once FVD has developed, the kidneys attempt to conserve body fluids, leading to a urine output of less than 1 mL/kg/h in an adult. Urine in this instance is concentrated and represents a healthy renal response. Daily body weights are monitored; an acute loss of 0.5 kg (1.1 lb) represents a fluid loss of approximately 500 mL (1 L of fluid weighs approximately 1 kg, or 2.2 lb). Vital signs are closely monitored. The nurse observes for a weak, rapid pulse and orthostatic hypotension (i.e., a decrease in systolic pressure exceeding 20 mm Hg when the patient moves from a lying to a sitting position. A decrease in body temperature often accompanies FVD, unless there is a concurrent infection. Skin and tongue turgor are monitored on a regular basis. In a healthy person, pinched skin immediately returns to its normal position when released (Weber & Kelley, 2014). This elastic property, referred to as turgor, is partially dependent on interstitial fluid volume. In a person with FVD, the skin flattens more slowly after the pinch is released. In a person with severe FVD, the skin may remain elevated for many seconds. Tissue turgor is best measured by pinching the skin over the sternum, inner aspects of the thighs, or forehead. Tongue turgor is not affected by age (see previous Gerontologic Considerations), and evaluating this may be more valid than evaluating skin turgor (Sterns, 2014a). In a normal person, the tongue has one longitudinal furrow. In the person with FVD, there are additional longitudinal furrows and the tongue is smaller because of fluid loss. The degree of oral mucous membrane moisture is also assessed; a dry mouth may indicate either FVD or mouth breathing. 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 be 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). Medical Surgical Nursing Fluids & Electrolytes 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 of 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 is 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 (Comeford, 2015; Frandsen & Pennington, 2014). 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 is so severely impaired that pharmacologic agents cannot act efficiently, other modalities are considered to remove sodium and 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 to as little as 250 mg of sodium per day, depending on the patient’s needs. A mild sodium-restricted diet allows only light salting of food (about half the usual amount) in cooking and at the table, and no addition of salt to commercially prepared foods that are already seasoned. Foods high in sodium must be avoided. It is the sodium salt (sodium chloride) rather than sodium itself that contributes to edema. Therefore, patients are instructed to read food labels carefully to determine salt content. Medical Surgical Nursing Fluids & Electrolytes 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 used cautiously by patients taking potassium-sparing diuretics (e.g., spironolactone, triamterene, amiloride). They should not be used in conditions associated with potassium retention, such as advanced renal disease. Salt substitutes containing ammonium chloride can be harmful to patients with liver damage. In some communities, drinking water may 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 be carefully examined for sodium content before purchasing and drinking bottled water. Also, patients on sodium-restricted diets should be 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+ (minimal) to 4+ (severe) (see Chapter 29, Fig. 29-2). Peripheral edema is monitored by measuring the circumference of the extremity with a tape marked in millimeters (Weber & Kelley, 2014). Medical Surgical Nursing Fluids & Electrolytes