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Fluid, Electrolyte, and Acid-Base Balance

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1 Fluid, Electrolyte, and Acid-Base Balance
Chapter 41 Fluid, Electrolyte, and Acid-Base Balance Fluid surrounds all the cells in the body and is also inside cells. Body fluids contain electrolytes such as sodium and potassium; they also have a certain degree of acidity. Fluid, electrolyte, and acid-base balances within the body maintain the health and function of all body systems. In this chapter, you will learn how the body normally maintains fluid, electrolyte, and acid-base balance. You also will learn how imbalances develop; how various fluid, electrolyte, and acid-base imbalances affect patients; and ways to help patients maintain or restore balance safely.

2 Characteristics of Body Fluids
Fluid = Water that contains dissolved or suspended substances such as glucose, mineral salts, and proteins. Fluid amount = Volume. Fluid concentration = Osmolality. Fluid composition (electrolyte concentration) Degree of acidity = pH The characteristics of body fluids influence body system function through their effects on cell function. All of these characteristics have regulatory mechanisms, which keep them in balance for normal function.

3 Scientific Knowledge Base : Location and Movement of Water and Electrolytes
Intracellular Fluid (ICF) = Fluids within cells ~2/3 of total body water Extracellular Fluid (ECF) = Fluid outside of cells ~1/3 of total body water Three divisions: – Interstitial – Intravascular – Transcellular •Body fluids containing water, Na+, and other electrolytes are distributed between distinct compartments: extracellular fluid (ECF) outside the cells, and intracellular fluid (ICF) inside the cells. •ECF fluids: Interstitial fluids are the fluids between cells and outside the blood vessels. These include lymph (fluid in the lymphatic channels). Intravascular fluid is blood plasma found in the vascular system. Transcellular fluids are secreted by epithelial cells and include cerebrospinal, pleural, peritoneal, and synovial fluids.

4 Body Fluid Compartments
[Shown is Figure 41-1 from text p. 883.]

5 Case Study Susan Reynolds, a 42-year-old married accountant, has just been admitted to the acute care unit with a history of nausea, loss of appetite, and vomiting and diarrhea for 7 days. She feels her symptoms are related to “bad food” she had on her recent business trip. Past medical history includes hypertension controlled by furosemide (Lasix) 40 mg by mouth once a day and a no-salt-added diet. [Ask the class: What fluid and electrolyte challenges does Susan face with her current illness? How does her medical history complicate management? Discuss.]

6 Electrolytes and Ions Electrolytes (mineral salts)
Compounds that separate into ions (charged particles) when they dissolve in water Ions (charged particles) Cations: positively charged Anions: negatively charged [Ask students to name some cations: sodium, potassium, calcium, magnesium.] [Ask students to name some anions: chloride, bicarbonate, sulfate.] Anions and cations combine to make salts. If you put table salt (NaCl) in water, it separates into Na+ and Cl−. Fluid that contains a large number of dissolved particles is more concentrated than the same amount of fluid that contains only a few particles. Osmolality of a fluid is a measure of the number of particles per kilogram of water. Electrolytes (solute) are dissolved in plasma (solution). The liquid in which a solute is dissolved is called a solvent. [Table 41-1 Laboratory Normal Values for Adults on text p. 883 identifies electrolytes and their normal values.]

7 Isotonic, Hypotonic, and Hypertonic Solutions
Solutions are classified as hypertonic, isotonic, or hypotonic. Particles that cannot cross cell membranes easily (called nonpermeant particles) determine the tonicity of a fluid. A fluid with the same concentration of nonpermeant particles as normal blood is called isotonic. Isotonic solutions have the same osmolarity as blood, similar to normal saline (0.9% sodium chloride). A hypotonic solution is more dilute than blood, and a hypertonic solution is more concentrated than normal blood. A hypertonic solution such as 3% sodium chloride pulls fluid from cells, causing them to shrink. A hypotonic solution such as 0.45% sodium chloride moves fluids into cells, causing them to enlarge. Some particles (e.g., urea) pass easily through cell membranes; others such as Na+ cannot cross easily. [Discuss what happens to the cell in each type of fluid and why.] [Shown is Figure 41-2 from text p. 884.]

8 Movement of Water and Electrolytes
Active transport Movement of ions against osmotic pressure to an area of higher pressure; requires energy Diffusion Passive movement of electrolytes or other particles down the concentration gradient (from higher to lower concentration) Osmosis Movement of water (or other solute) from an area of lesser to one of greater concentration Filtration Movement across a membrane, under pressure, from higher to lower pressure Active transport requires energy in the form of adenosine triphosphate (ATP) to move electrolytes across cell membranes against the concentration gradient (from areas of lower concentration to areas of higher concentration). It is enhanced by carrier molecules within a cell that bind themselves to incoming molecules. One example of active transport is the sodium-potassium pump, which moves Na+ out of a cell and K+ into it, keeping ICF lower in Na+ and higher in K+ than ECF. Diffusion is affected by molecular size, concentration, and temperature of a solution. The difference between two concentrations is known as the concentration gradient. Diffusion is passive movement of electrolytes or other particles down the concentration gradient (from areas of higher concentration to areas of lower concentration). Within a body compartment, electrolytes diffuse easily by random movements until the concentration is the same in all areas. Fluids and electrolytes shift from compartment to compartment, and compartments are separated by cell walls and capillary membranes. Osmosis attempts to equalize concentrations of molecules (ions) on both sides of the membrane. Osmotic pressure is the drawing power of water and depends on the number of molecules in solution. [Osmosis is discussed in detail on the next slide.] Hydrostatic pressure is the force of the fluid pressing outward against a surface. In the process of filtration, hydrostatic pressure differences determine the movement of water. With increased hydrostatic pressure on the venous side of the capillary bed, edema will occur. However, diffusion of electrolytes across cell membranes requires proteins that serve as ion channels. For example, when a sodium channel in a cell membrane is open, Na+ diffuses passively across the cell membrane into the ICF because concentration is lower in the ICF. Opening of ion channels is tightly controlled and plays an important part in muscle and nerve function.

9 Osmosis Osmosis moves water through a semi-permeable membrane.
Water moves across cell membranes by osmosis, a process by which water moves through a membrane that separates fluids with different particle concentrations. Cell membranes are semi-permeable, which means that water crosses them easily, but they are not freely permeable to many types of particles, including electrolytes such as sodium and potassium. These semi-permeable cell membranes separate interstitial fluid from ICF. The fluid in each of these compartments exerts osmotic pressure, an inward-pulling force caused by particles in the fluid. Particles already inside the cell exert ICF osmotic pressure, which tends to pull water into the cell. Particles in the interstitial fluid exert interstitial fluid osmotic pressure, which tends to pull water out of the cell. Water moves into the compartment that has a higher osmotic pressure (inward-pulling force) until the particle concentration is equal in the two compartments. If the particle concentration in the interstitial compartment changes, osmosis occurs rapidly and moves water into or out of cells to equalize osmotic pressures. For example, when a hypotonic solution (more dilute than normal body fluids) is administered intravenously, it dilutes the interstitial fluid, decreasing its osmotic pressure to below intracellular osmotic pressure. Water moves rapidly into cells until the two osmotic pressures are equal again. On the other hand, infusion of a hypertonic intravenous (IV) solution (more concentrated than normal body fluids) causes water to leave cells by osmosis to equalize the osmolality between interstitial and intracellular compartments. [Shown is Figure 41-3 from text p. 884.]

10 Filtration Capillary filtration moves fluid between vascular and interstitial compartments. Fluid moves into and out of capillaries (between vascular and interstitial compartments) by the process of filtration. Filtration is the net effect of four forces—two that tend to move fluid out of capillaries and small venules, and two that tend to move fluid back into them. Hydrostatic pressure is the force of the fluid pressing outward against a surface. Similarly, capillary hydrostatic pressure is a relatively strong outward-pushing force that helps move fluid from capillaries into the interstitial area. Interstitial fluid hydrostatic pressure is a weaker opposing force that tends to push fluid back into capillaries. Blood contains albumin and other proteins known as colloids. Colloid proteins of blood are much larger than electrolytes, glucose, and other molecules that dissolve easily. Most colloids are too large to leave capillaries in the fluid that is filtered, so they remain in the blood. Because they are particles, colloids exert osmotic pressure. Blood colloid osmotic pressure, also called oncotic pressure, is an inward-pulling force caused by blood proteins that helps move fluid from the interstitial area back into capillaries. Interstitial fluid colloid osmotic pressure normally is a very small opposing force. At the arterial end of a normal capillary, capillary hydrostatic pressure is strongest, and fluid moves from the capillary into the interstitial area, bringing nutrients to cells. At the venous end, capillary hydrostatic pressure is weaker, and the colloid osmotic pressure of the blood is stronger. Thus fluid moves into the capillary at the venous end, removing waste products from cellular metabolism. Lymph vessels remove any extra fluid and proteins that have leaked into the interstitial fluid. Disease processes and other factors that alter these forces may cause accumulation of excess fluid in the interstitial space, known as edema. Inflammation is another cause of edema. It increases capillary blood flow and allows capillaries to leak colloids into the interstitial space. The resulting increased capillary hydrostatic pressure and increased interstitial colloid osmotic pressure produce localized edema in the inflamed tissues. [Shown is Figure 41-4 from text p. 885.]

11 Fluid Balance Fluid balance consists of Fluid intake
Fluid intake and absorption Fluid distribution Fluid output Fluid intake Drinking and foods Thirst and habit Fluid distribution = Movement of fluid among its various compartments. Fluid homeostasis is the dynamic interplay of three processes: fluid intake and absorption, fluid distribution, and fluid output. Human total daily fluid output consists of hypotonic sodium-containing fluid. People must have intake of an equivalent amount of hypotonic sodium-containing fluid (or water plus foods with some salt) to maintain fluid balance. Fluid intake occurs orally through drinking but also through eating because most foods contain some water. Food metabolism creates additional water. Average fluid intake from these routes for healthy adults is about 2300 mL, although it varies widely. Other routes of fluid intake include IV, rectal (e.g., enemas), and irrigation of body cavities that can absorb fluid. Although you might think that the major regulator of oral fluid intake is thirst, habit and social reasons actually account for most fluid intake. Thirst, the conscious desire for water, is an important regulator of fluid intake when plasma osmolality increases (osmoreceptor-mediated thirst) or blood volume decreases (baroreceptor-mediated thirst and angiotensin II– and III–mediated thirst). (Thirst is discussed further on the next slide.) Fluid distribution between extracellular and intracellular compartments occurs by osmosis. Fluid distribution between blood vessels and interstitial portions of the ECF occurs by filtration. [Review Table 41-2 on text p. 884 Healthy Adult Average Daily Fluid Intake and Output.]

12 Case Study (cont’d) Robert is a junior nursing student assigned to Mrs. Reynolds. He has cared for other patients with gastrointestinal problems but never one with fluid and electrolyte problems. Robert plans his care by reviewing Mrs. Reynolds’ chart and her health care provider’s orders. [Ask the class: What will Robert discover about the patient based on her history? The patient’s history reveals that she is at risk for a fluid and electrolyte imbalance from a GI disturbance and continued use of a diuretic.]

13 Thirst Mechanism This diagram shows stimuli that affect the thirst mechanism. The thirst control mechanism is located within the hypothalamus in the brain. Osmoreceptors continually monitor plasma osmolality; when it increases, they cause thirst by stimulating neurons in the hypothalamus. Dry oral mucous membranes also cause thirst. People who are alert can obtain fluid or communicate their thirst to others, and fluid intake restores fluid balance. Infants, patients with neurological or psychological problems, and some older adults who are unable to perceive or communicate their thirst are at risk for dehydration. [Shown is Figure 41-5 from text p. 886.]

14 Fluid Balance Fluid output Normally via skin, lungs, GI tract, kidneys
Abnormally via vomiting, wound drainage, hemorrhage Influenced by Antidiuretic hormone (ADH) Renin-angiotensin-aldosterone system (RAAS) Atrial natriuretic peptides (ANPs) [Table 41-2 on text p. 885 Healthy Adult Average Daily Fluid Intake and Output shows average amounts of fluid excretion for healthy adults, although urine output varies greatly, depending on fluid intake.] Insensible (not visible) water loss through the skin and lungs is continuous. It increases when a person has a fever or a recent burn to the skin. Sweat, which is visible and contains sodium, occurs intermittently and increases fluid output substantially. The GI tract plays a vital role in fluid balance. Approximately 3 to 6 L of fluid moves into the GI tract daily and then returns again to the ECF. The average adult normally excretes only 100 mL of fluid each day through feces. However, diarrhea causes a large fluid output from the GI tract. The kidneys are the major regulators of fluid output because they respond to hormones that influence urine production. When healthy adults drink more water, they increase urine production to maintain fluid balance. If they drink less water, sweat a lot, or lose fluid by vomiting, their urine volume decreases to maintain fluid balance. These adjustments primarily are caused by the actions of antidiuretic hormone (ADH), the renin-angiotensin-aldosterone system (RAAS), and atrial natriuretic peptides (ANPs). ADH regulates the osmolality of body fluids by influencing how much water is excreted in urine. The RAAS regulates ECF volume by influencing how much sodium and water is excreted in urine. Atrial natriuretic peptide (ANP) also regulates ECF volume by influencing how much sodium and water is excreted in urine.

15 Hormones Influencing Fluid Output
Major hormones that influence renal fluid excretion. A, Antidiuretic hormone (ADH). B, Aldosterone. C, Atrial natriuretic peptide (ANP). ADH is synthesized by neurons in the hypothalamus that release it from the posterior pituitary gland. ADH circulates in the blood to the kidneys, where it acts on the collecting ducts. Its name—antidiuretic hormone—tells you what it does. It causes renal cells to resorb water, taking water from the renal tubular fluid and putting it back in the blood. This action decreases urine volume, concentrating the urine while diluting the blood by adding water to it. People normally have some ADH release to maintain fluid balance. More ADH is released if body fluids become more concentrated. Factors that increase ADH levels include severely decreased blood volume (e.g., dehydration, hemorrhage), pain, stressors, and some medications. ADH levels decrease if body fluids become too dilute. This allows more water to be excreted in urine, creating a larger volume of dilute urine and concentrating the body fluids back to normal osmolality. For example, ethyl alcohol decreases ADH release, which causes people to urinate frequently when they drink alcoholic beverages. The renin-angiotensin-aldosterone system (RAAS) regulates ECF volume by influencing how much sodium and water is excreted in urine. It also contributes to regulation of blood pressure. Specialized cells in the kidneys release the enzyme renin, which acts on angiotensinogen, an inactive protein secreted by the liver that circulates in the blood. Renin converts angiotensinogen to angiotensin I, which other enzymes in the lung capillaries convert to angiotensin II. Angiotensin II has several functions, one of which is vasoconstriction in some vascular beds. Important fluid homeostasis functions of angiotensin II include stimulation of aldosterone release from the adrenal cortex. Aldosterone circulates to the kidneys, where it causes resorption of sodium and water in isotonic proportion in the distal renal tubules. Removing sodium and water from the renal tubules and returning it to the blood increases the volume of the ECF. Aldosterone also contributes to electrolyte and acid-base balance by increasing urinary excretion of potassium and hydrogen ions. To maintain fluid balance, normally some action of the RAAS occurs. Certain stimuli increase or decrease the activity of this system to restore fluid balance. For example, if hemorrhage or vomiting decreases the extracellular fluid volume (ECV), blood flow decreases through the renal arteries, and more renin is released. This increased RAAS activity causes more sodium and water retention, helping to restore ECV. Atrial natriuretic peptide (ANP) also regulates ECV by influencing how much sodium and water is excreted in urine. Cells in the atria of the heart release ANP when they are stretched (e.g., by increased ECV). ANP is a weak hormone that inhibits ADH by increasing the loss of sodium and water in the urine. Thus ANP opposes the effect of aldosterone. [Shown is Figure 41-6 from text p. 886.]

16 Fluid Balance (cont’d)
Fluid intake Thirst regulates fluid intake ~2300 mL/day Fluid distribution Extracellular and intracellular Vascular and interstitial Hormonal Influences Antidiuretic hormone Renin-angiotensin-aldosterone mechanism Atrial natriuretic peptides Fluid output Through kidneys, skin, lungs, and GI tract Insensible loss Sensible loss This slide summarizes the components of fluid balance.

17 Quick Quiz! 1. A patient is diaphoretic and has an oral temperature of 104° F. These are classic signs of A. ADH deficit. B. Extracellular fluid loss. C. Insensible water loss. D. Sensible water loss. Answer: D

18 Fluid Imbalances Extracellular fluid volume imbalances
Extracellular fluid volume (ECV) deficit Hypovolemia means decreased vascular volume and often is used when discussing ECV deficit. ECV excess Osmolality imbalances Hypernatremia, “water deficit”; hypertonic Hyponatremia, “water excess”; hypotonic Clinical dehydration = ECV deficit and hypernatremia combined If disease processes, medications, or other factors disrupt fluid intake or output, imbalances sometimes occur. For example, with diarrhea, fluid output is increased, and a fluid imbalance (dehydration) occurs if fluid intake does not increase appropriately. Two major types of fluid imbalances are known: volume imbalances and osmolality imbalances. Volume imbalances are disturbances of the amount of fluid in the extracellular compartment. Osmolality imbalances are disturbances of the concentration of body fluids. Volume and osmolality imbalances may occur separately or in combination. With an ECV imbalance, too little (ECV deficit) or too much (ECV excess) isotonic fluid is present. •ECV deficit and excess are abnormal volumes of isotonic fluid, manifested as sudden changes in body weight and changes in markers of vascular and interstitial volume. ECV deficit is present when isotonic fluid is insufficient in the extracellular compartment. Remember that a lot of sodium is found in normal ECF. With ECV deficit, output of isotonic fluid exceeds intake of sodium-containing fluid. Because ECF is both vascular and interstitial, signs and symptoms arise from lack of volume in both of these compartments. ECV excess occurs when too much isotonic fluid is found in the extracellular compartment. Intake of sodium-containing isotonic fluid has exceeded fluid output. For example, when you eat more salty foods than usual and drink water, you may notice that your ankles swell or rings on your fingers feel tight, and you gain 2 lbs (1 kg) or more overnight. These are manifestations of mild ECV excess. In an osmolality imbalance, body fluids become hypertonic or hypotonic, and this causes osmotic shifts of water across cell membranes. Osmolality imbalances are called hypernatremia and hyponatremia. •Osmolality imbalances are abnormal concentrations of body fluids, manifested as altered serum Na+ levels and decreased level of consciousness. Hypernatremia, also called water deficit, is a hypertonic condition. One of two general causes make body fluids too concentrated: loss of relatively more water than salt, or gain of relatively more salt than water. When the interstitial fluid becomes hypertonic, water leaves cells by osmosis, and they shrivel. Signs and symptoms of hypernatremia are those of cerebral dysfunction, which arise when brain cells shrivel. Hyponatremia, also called water excess or water intoxication, is a hypotonic condition. It arises from gain of relatively more water than salt or loss of relatively more salt than water. The excessively dilute condition of interstitial fluid causes water to enter cells by osmosis, causing the cells to swell. Signs and symptoms of cerebral dysfunction occur when brain cells swell. ECV deficit and hypernatremia often occur at the same time; this combination is called clinical dehydration. The ECV is too low, and the body fluids are too concentrated. Clinical dehydration is common with gastroenteritis or other causes of severe vomiting and diarrhea when people are not able to replace their fluid output with enough intake of dilute sodium-containing fluids. Signs and symptoms of clinical dehydration are those of both ECV deficit and hypernatremia. •Treatment for ECV excess consists of Na+ restriction and fluid restriction, if severe; treatment for hyponatremia usually involves water restriction. [Review Table 41-3 on text p. 888 Fluid Imbalances.]

19 Fluid Volume and Osmolality Imbalances
[Review each imbalance and its parallel in health and disease.] [Shown is Figure 41-7 from text p. 887.]

20 Electrolyte Balance Intake and absorption Distribution Output
Plasma concentrations of K+, Ca2+, Mg+, and phosphate (Pi) are very low compared with their concentrations in cells and bone. Concentration differences are necessary for normal muscle and nerve function. Output Urine, feces, and sweat Vomiting, drainage, and fistulas You can best understand electrolyte balance by considering the three processes involved in electrolyte homeostasis: electrolyte intake and absorption, electrolyte distribution, and electrolyte output. •Interplay of electrolyte intake and absorption, electrolyte distribution, and electrolyte output determines the balance of K+, Ca2+, Mg2+, and phosphate. Intake comes from foods and beverages. Some substances enhance or hinder electrolyte absorption. Although sodium is an electrolyte, it is not included here because serum sodium imbalances are the osmolality imbalances discussed previously. Electrolyte distribution is an important issue. Note that the electrolyte values that you review from laboratory reports are measured in blood serum and do not measure intracellular levels. Electrolyte output occurs through normal excretion in urine, feces, and sweat. Output also occurs through vomiting, drainage tubes, and fistulas. When electrolyte output increases, electrolyte intake must increase to maintain electrolyte balance. Similarly, if electrolyte output decreases, as with oliguria, electrolyte intake must also decrease to maintain balance. [Review Table 41-4 on text p. 889 Electrolyte Intake and Absorption, Distribution, and Output.]

21 Electrolyte Imbalances
Potassium (K+) Hypokalemia Hyperkalemia Calcium (Ca2+) Hypocalcemia Hypercalcemia Magnesium (Mg2+) Hypomagnesemia Hypermagnesemia (Hypernatremia and hyponatremia were discussed with osmolality imbalances.) [Ask the class to use their knowledge of word origins to analyze the terms on the slide. Discuss that -emia means blood condition; hyper- means excessive; hypo- means deficient; and the three word roots (kal, calc, and magnes) represent the three elements potassium, calcium, and magnesium.] Factors such as diarrhea, endocrine disorders, and medications that disrupt electrolyte homeostasis cause electrolyte imbalances. Electrolyte intake greater than electrolyte output or a shift of electrolytes from cells or bone into the ECF causes plasma electrolyte excess. Electrolyte intake less than electrolyte output or shift of electrolyte from the ECF into cells or bone causes plasma electrolyte deficit. Hypokalemia is abnormally low potassium concentration in the blood. Hypokalemia results from decreased potassium intake and absorption, a shift of potassium from the ECF into cells, and an increased potassium output. Common causes of hypokalemia from increased potassium output include diarrhea, repeated vomiting, and use of potassium-wasting diuretics. People who have these conditions need to increase their potassium intake to reduce their risk of hypokalemia. Hypokalemia causes muscle weakness, which becomes life threatening if it includes respiratory muscles and potentially life-threatening cardiac dysrhythmias. Hyperkalemia is abnormally high potassium ion concentration in the blood. Its general causes are increased potassium intake and absorption, shift of potassium from cells into the ECF, and decreased potassium output. People who have oliguria (decreased urine output) are at high risk of hyperkalemia from the resultant decreased potassium output unless their potassium intake also decreases substantially. Understanding this principle helps you remember to check urine output before you administer IV solutions containing potassium. Hyperkalemia can cause muscle weakness, potentially life-threatening cardiac dysrhythmias, and cardiac arrest. Hypocalcemia is abnormally low calcium concentration in the blood. The physiologically active form of calcium in the blood is ionized calcium. Total blood calcium also contains inactive forms that are bound to plasma proteins and small anions such as citrate. Factors that cause too much ionized calcium to shift to bound forms cause symptomatic ionized hypocalcemia. People who have acute pancreatitis frequently develop hypocalcemia because calcium binds to undigested fat in their feces and is excreted. This process decreases absorption of dietary calcium and increases calcium output by preventing resorption of calcium contained in GI fluids. Hypocalcemia increases neuromuscular excitability, which is the basis for its signs and symptoms. Hypercalcemia is abnormally high calcium concentration in the blood. Hypercalcemia results from increased calcium intake and absorption, shift of calcium from bones into the ECF, and decreased calcium output. Patients with cancer often develop hypercalcemia because some cancer cells secrete chemicals into the blood that are related to parathyroid hormone. When these chemicals reach the bones, they cause shift of calcium from bones into the ECF. This weakens bones, and the person sometimes develops pathological fractures (i.e., bone breakage caused by forces that would not break a healthy bone). Hypercalcemia decreases neuromuscular excitability, the basis for its other signs and symptoms, the most common of which is lethargy. Hypomagnesemia is abnormally low magnesium concentration in the blood. Its general causes include decreased magnesium intake and absorption, shift of plasma magnesium to its inactive bound form, and increased magnesium output. Signs and symptoms are similar to those of hypocalcemia because hypomagnesemia also increases neuromuscular excitability. Hypermagnesemia is abnormally high magnesium concentration in the blood. End-stage renal disease causes hypermagnesemia unless the person decreases magnesium intake to match the decreased output. Signs and symptoms are caused by decreased neuromuscular excitability, with lethargy and decreased deep tendon reflexes being most common. [Review Table 41-5 from text pp Electrolyte Imbalances.]

22 Case Study (cont’d) Mrs. Reynolds’ physician has admitted her for observation and has obtained a blood sample for electrolyte levels, CBC, and an ECG. Orders include nothing by mouth, an IV infusion of 0.9% saline at 125 mL/hr, intake and output (I&O) recordings, and vital signs every 4 hours, in addition to daily weights. What assessment activities do you anticipate Robert will perform? [Discuss: Ask Mrs. Reynolds to describe her nausea and what accompanying signs and symptoms she is experiencing. Conduct an examination of GI and urinary function. Assess her vital signs. Assess Mrs. Reynolds’ skin and mucous membranes for indicators of dehydration. Evaluation her laboratory vales and ECG results.]

23 Acid-Base Balance Acid production, buffering, and excretion interplay to create balance. Acids release hydrogen (H+) ions; bases (alkaline substances) take up H+ ions. Degree of acidity is reported as pH. pH scale: 1.0 (very acid) to 14.0 (very base) pH of 7.0 is neutral; normal arterial blood is 7.35 to 7.45. Maintaining pH within this normal range is very important for optimal cell function. For optimal cell function, the body maintains a balance between acids and bases. Acid-base homeostasis is the dynamic interplay of three processes: acid production, acid buffering, and acid excretion. Normal acid-base balance is maintained with acid excretion equal to acid production. The more H+ ions that are present, the more acidic is the solution. The degree of acidity in blood and other body fluids is reported from the clinical laboratory as pH. If pH goes outside the normal range, enzymes within cells do not function properly; hemoglobin does not manage oxygen properly; and serious physiological problems, including death, may occur. Laboratory tests of a sample of arterial blood called arterial blood gases (ABGs) are used to monitor a patient’s acid-base balance. [Review Table 41-6 on text p. 892 Arterial Blood Gas Measures.]

24 Acid-Base Balance (cont’d)
Acid production CO2 +H2O ↔ H2CO3 ↔ H+ + HCO3− Carbon dioxide + water ↔ Carbonic acid ↔ Hydrogen ion + Bicarbonate Acid buffering: Buffers are pairs of chemicals that work together to maintain normal pH of body fluids HCO3− + H+ ↔ H2CO3 Bicarbonate + Hydrogen ion ↔ Carbonic acid H2CO3 ↔ H+ + HCO3− Carbonic acid ↔ Hydrogen ion + Bicarbonate Production: Cellular metabolism constantly creates two types of acids: carbonic acid and metabolic acids. Cells produce carbon dioxide (CO2), which acts as an acid in the body by converting to carbonic acid. Metabolic acids are any acids that are not carbonic acid. They include citric acid, lactic acid, and many others. Buffering: If too many free H+ ions are present, a buffer takes them up, so they no longer are free. If too few are present, a buffer can release H+ ions to prevent an acid-base imbalance. Buffers work rapidly—within seconds. All body fluids contain buffers. The major buffer in ECF is the bicarbonate (HCO3−) buffer system, which buffers metabolic acids. It consists of a lot of bicarbonate and a small amount of carbonic acid (normally a 20:1 ratio). Addition of H+ released by a metabolic acid to a bicarbonate ion makes more carbonic acid. Now the H+ is no longer free and will not decrease the blood pH (see slide for green equation). If too few H+ ions are present, the carbonic acid portion of the buffer pair will release some, increasing the bicarbonate, again returning pH to normal (see slide for bottom two blue equations). Other buffers include hemoglobin, protein buffers, and phosphate buffers. Cellular and bone buffers also contribute. Buffers normally keep the blood from becoming too acid when acids that are produced by cells circulate to the lungs and kidneys for excretion.

25 Acid-Base Balance (cont’d)
Acid excretion systems: lungs and kidneys Lungs excrete carbonic acid. Kidneys excrete metabolic acids. Excretion of carbonic acid When you exhale, you excrete carbonic acid in the form of CO2 and water. Excretion of metabolic acids The kidneys excrete all acids except carbonic acid. The body has two acid excretion systems: lungs and kidneys. The lungs excrete carbonic acid; the kidneys excrete metabolic acids. When you exhale, you excrete carbonic acid in the form of CO2 and water. If the PaCO2 (i.e., level of CO2 in the blood) rises, the chemoreceptors trigger faster and deeper respirations to excrete the excess. If the PaCO2 falls, the chemoreceptors trigger slower and shallower respirations, so more of the CO2 produced by cells remains in the blood and makes up the deficit. These alterations in respiratory rate and depth maintain the carbonic acid portion of acid-base balance. Sometimes people who have lung disease have difficulty with normal excretion of carbonic acid, which causes it to accumulate and make the blood more acid. The kidneys excrete all acids except carbonic acid. They secrete H+ into the renal tubular fluid, putting HCO3− back into the blood at the same time. If too many H+ ions are present in the blood, renal cells move more H+ ions into the renal tubules for excretion, retaining more HCO3− in the process. If too few H+ ions are present in the blood, renal cells secrete fewer H+ ions. Phosphate buffers in the renal tubular fluid keep the urine from becoming too acidic when the kidneys excrete H+ ions. If the kidneys need to excrete a lot of H+, renal tubular cells secrete ammonia, which combines with H+ ions in the tubules to make NH4+, ammonium ions. Buffering by phosphate and the creation of NH4+ turn free H+ ions into other molecules in the renal tubular fluid. This process enables metabolic acid excretion in urine without making urine too acidic. People who have kidney disease often have difficulty with normal excretion of metabolic acids.

26 Acid Production and Excretion
This diagram shows acid production and excretion. [Shown is Figure 41-8 from text p. 892.]

27 Quick Quiz! 2. The body’s fluid and electrolyte balance is maintained partially by hormonal regulation. You will express an understanding of this mechanism in which of the following statements? A. “The pituitary secretes aldosterone.” B. “The kidneys secrete antidiuretic hormone.” C. “The adrenal cortex secretes antidiuretic hormone.” D. “The pituitary gland secretes antidiuretic hormone.” Answer: D

28 Acid-Base Imbalances Types of acidosis: respiratory and metabolic
Types of alkalosis: respiratory and metabolic Respiratory acidosis Arises from alveolar hypoventilation Lungs unable to excrete enough CO2 Excess carbonic acid in the blood decreases pH. Respiratory alkalosis Arises from alveolar hyperventilation Lungs excrete too much CO2 Deficit of carbonic acid in the blood increases pH. People develop acid-base imbalances when their normal homeostatic mechanisms are dysfunctional or overwhelmed. The term acidosis describes a condition that tends to make the blood relatively too acidic. Because our cells produce two types of acid, two different types of acidosis have been identified: respiratory acidosis and metabolic acidosis. The term alkalosis describes a condition that tends to make the blood relatively too basic (alkaline). Two types of alkalosis are known: respiratory alkalosis and metabolic alkalosis. The body has compensatory mechanisms that limit the extent of pH change with acid-base imbalances. It is important to remember that the kidney or lung cannot compensate for itself. Therefore the kidneys compensate for respiratory acid-base imbalances, and the respiratory system compensates for metabolic acid-base imbalances. These compensatory mechanisms do not correct the problem, but they assist the body to adapt. However, if the underlying condition is not corrected, these compensatory mechanisms will fail. [Review Table 41-7 on text p. 894 Acid-Base Imbalances.] •Respiratory acidosis arises from alveolar hypoventilation; the lungs are unable to excrete enough CO2. The PaCO2 rises, creating an excess of carbonic acid in the blood, which decreases pH. The kidneys compensate by increasing excretion of metabolic acids in the urine, which increases blood bicarbonate. This compensatory process is slow, often taking 24 hours to show clinical effect and 3 to 5 days to reach steady state. Decreased cerebrospinal fluid (CSF) pH and intracellular pH of brain cells cause decreased levels of consciousness. •Respiratory alkalosis arises from alveolar hyperventilation; the lungs excrete too much carbonic acid (CO2 and water). The PaCO2 falls, creating a deficit of carbonic acid in the blood, which increases pH. Respiratory alkalosis usually is short lived; thus the kidneys do not have time to compensate. When the pH of blood, CSF, and ICF increases acutely, cell membrane excitability also increases, giving rise to neurological symptoms such as excitement, confusion, and paresthesias. If the pH rises enough, central nervous system (CNS) depression can occur.

29 Acid-Base Imbalances (cont’d)
Metabolic acidosis Arises from increase in metabolic acid or decrease in base (bicarbonate) Kidneys unable to excrete enough metabolic acids, which accumulate in the blood Results in decreased level of consciousness Metabolic alkalosis Arises from direct increase in base (bicarbonate) or decrease in metabolic acid Results in increased blood bicarbonate Metabolic acidosis occurs from an increase in metabolic acid or a decrease in base (bicarbonate). The kidneys are unable to excrete enough metabolic acids, which accumulate in the blood, or bicarbonate is removed from the body directly, as with diarrhea. In either case, the blood HCO3− decreases, and the pH falls. With an increase in metabolic acids, blood HCO3− decreases because it is used to buffer metabolic acids. Similarly, when patients have conditions that cause the removal of HCO3−, the amount of HCO3− in the blood decreases. To help identify the specific cause, health care providers and the laboratory calculate the anion gap, a reflection of unmeasured anions in plasma. You calculate anion gap by subtracting the sum of plasma concentrations of the anions Cl− and HCO3− from the plasma concentration of the cation Na+. When reviewing laboratory reports, check the reference values from the laboratory that measured the electrolyte concentrations. [Review Table 41-8 from text p. 895 Anion Gap in Metabolic Acidosis.] The abnormally low pH in metabolic acidosis stimulates the chemoreceptors, so the respiratory system compensates for the acidosis by hyperventilation. Compensatory hyperventilation begins in a few minutes and removes carbonic acid from the body. This process does not correct the problem, but it helps limit the pH decrease. Metabolic acidosis decreases one’s level of consciousness. Metabolic alkalosis occurs from a direct increase in base (HCO3−) or a decrease in metabolic acid, which increases blood HCO3− by releasing it from its buffering function. Common causes include vomiting and gastric suction. The respiratory compensation for metabolic alkalosis is hypoventilation. The decreased rate and depth of respiration allow carbonic acid to increase in the blood, as can be seen by an increased PaCO2. The need for oxygen may limit the degree of respiratory compensation for metabolic alkalosis. Because HCO3− crosses the blood-brain barrier with difficulty, neurological signs and symptoms are less severe or even absent with metabolic alkalosis.

30 Acid-Base Imbalances (cont’d)
Kidney or lung cannot compensate for itself. Kidneys compensate for respiratory imbalances. Respiratory system compensates for metabolic imbalances. These compensatory mechanisms do not correct the problem, but they assist the body in adapting. However, if the underlying condition is not corrected, these compensatory mechanisms will fail. Recall that the kidney or lung cannot compensate for itself. Therefore the kidneys compensate for respiratory acid-base imbalances; the respiratory system compensates for metabolic acid-base imbalances. Acid-base imbalances are caused by excesses or deficits of carbonic or metabolic acids, manifested as changes in level of consciousness and abnormalities of PaCO2, HCO3−, and pH.

31 Nursing Knowledge Base
Use the scientific knowledge base in clinical decision making to provide safe, optimal fluid therapy. Apply knowledge of risk factors for fluid imbalances and physiology of normal aging when assessing older adults, knowing that this age group is at high risk for fluid imbalances. Ask questions to elicit risk factors for fluid, electrolyte, and acid-base imbalances. Perform clinical assessments for signs and symptoms of these imbalances. You will apply knowledge about fluid, electrolyte, and acid-base imbalance in many clinical settings. You will incorporate nursing and collaborative interventions to maintain or restore fluid and electrolyte balance. Skills and techniques for safe IV therapy are a vital area of the nursing knowledge base and the focus of much nursing research to support evidence-based practice.

32 Nursing Process: Assessment
Nursing history Age: very young and old at risk Environment: excessively hot? Dietary intake: fluids, salt, foods rich in potassium, calcium, and magnesium Lifestyle: alcohol intake history Medications: include over-the-counter (OTC) and herbal, in addition to prescription medications Using a systematic approach in assessment enables you to help patients safely maintain or restore fluid, electrolyte, and acid-base balances. A patient’s fluid, electrolyte, or acid-base imbalance is sometimes so severe that it prevents initial discussion of his or her expressed needs, values, and preferences. However, when a patient is alert enough to discuss care, you need to elicit this information. Focus on the patient’s experience with fluid, electrolyte, or acid-base alterations and his or her perceptions of the illness. Ask about the patient’s greatest concerns regarding fluid status to build the basis for active partnership in planning, implementing, and evaluating patient-centered care. Clinical assessment begins with a patient history designed to reveal risk factors that cause or contribute to fluid, electrolyte, and acid-base imbalances. Ask specific, focused questions to identify factors that contribute to a patient’s potential imbalances. First, assess a patient’s age. Infants are at greater risk for ECV deficit and hypernatremia because body water loss is proportionately greater per kilogram of weight. Fluctuations in fluid balance are greater in adolescent girls because of hormonal changes associated with the menstrual cycle. Older adults experience a number of age-related changes that potentially affect fluid, electrolyte, and acid-base balances. They often have more difficulty recovering from imbalances resulting from the combined effects of normal aging, various disease conditions, and multiple medications. Excessive sweating without adequate replacement of salt and water can lead to ECV deficit, hypernatremia, or clinical dehydration. Ask patients about their normal level of physical work, and whether they engage in vigorous exercise in hot environments. Do these patients have fluid replacements containing salt available during exercise and activity? Assess dietary intake of fluids; salt; and foods rich in potassium, calcium, and magnesium. Ask patients if they follow weight loss diets. Starvation diets and those with high fat and no carbohydrate content often lead to metabolic acidosis. In addition, assess the patient’s ability to chew and swallow, which, if altered, interferes with adequate intake of electrolyte-rich foods and fluids. Take an alcohol intake history. Chronic alcohol abuse commonly causes hypomagnesemia, in part because it increases renal magnesium excretion. Obtain a complete list of your patient’s current medications, including over-the-counter (OTC) and herbal preparations, to assess the risks for fluid, electrolyte, and acid-base imbalances. Use a drug reference book or a reputable online database to check the potential effects of other medications. Ask specifically about the use of baking soda as an antacid, which can cause ECV excess because of its high sodium content that holds water in the extracellular compartments. For an individual who uses laxatives, ask about the consistency and frequency of stools. Multiple loose stools remove fluid and electrolytes from the body, thus causing numerous imbalances. [See Figure 41-9 on text p. 895 Critical thinking model for fluid, electrolyte, and acid-base balances assessment; Table 41-9 on text p. 896 Risk Factors for Fluid, Electrolyte, and Acid-Base Imbalances; Box 41-1 on text p. 896 Nursing Assessment Questions; Box 41-2 on text p. 897 Focus on Older Adults: Factors Affecting Fluid, Electrolyte, and Acid-Base Balance; and Box 41-3 on text p. 897 Commonly Used Medications That Cause Fluid, Electrolyte, and Acid-Base Imbalances.]

33 Nursing Process: Assessment (cont’d)
Medical history Recent surgery (physiological stress) Gastrointestinal output Acute illness or trauma Respiratory disorders Burns Trauma Chronic illness Cancer Heart failure Oliguric renal disease •Patients who are very young or very old, whose intake and output (I&O) of fluid and/or electrolytes are not equal, or who have various chronic diseases or trauma are at high risk for fluid, electrolyte, and acid-base imbalances. Surgery causes a physiological stress response, which increases with extensive surgery and blood loss. On the second to fifth postoperative days, increased secretion of aldosterone, glucocorticoids, and ADH causes increased ECV, decreased osmolality, and increased potassium excretion. In otherwise healthy patients, these imbalances resolve without difficulty, but patients who have preexisting illnesses or additional risk factors often need treatment during this time period. Increased output of fluid through the GI tract is a common and important cause of fluid, electrolyte, and acid-base imbalances that requires careful assessment. Many acute respiratory disorders predispose patients to respiratory acidosis. For example, bacterial pneumonia causes alveoli to fill with exudate that impairs gas exchange, causing the patient to retain carbon dioxide, which leads to increased PaCO2 and respiratory acidosis. Burns place patients at high risk for ECV deficit from numerous mechanisms, including plasma-to-interstitial fluid shift and increased evaporative and exudate output. The greater the body surface burned, the greater is the fluid loss. Hemorrhage from any type of trauma causes ECV deficit from blood loss. Some types of trauma create additional risks. Chronic illness. Many chronic diseases create ongoing risks of fluid, electrolyte, and acid-base imbalances. In addition, the treatment regimens for chronic disease often cause imbalances. The types of fluid and electrolyte imbalances that occur with cancer depend on the type and progression of the cancer and treatment regimen. Patients who have chronic heart failure have diminished cardiac output, which reduces kidney perfusion and activates the RAAS. The action of aldosterone on the kidneys causes ECV excess and risk of hypokalemia. Most diuretics used to treat heart failure increase the risk of hypokalemia while reducing the ECV excess. Dietary sodium restriction is important with heart failure because Na+ holds water in the ECF, making the ECV excess worse. In severe heart failure, restriction of both fluid and sodium is prescribed to decrease the workload of the heart by reducing excess circulating fluid volume. Oliguria occurs when the kidneys have a reduced capacity to make urine. Some conditions, such as acute nephritis, cause a sudden onset of oliguria, whereas other problems, such as chronic kidney disease, lead to chronic oliguria. Oliguric renal disease prevents normal excretion of fluid, electrolytes, and metabolic acids, resulting in ECV excess, hyperkalemia, hypermagnesemia, hyperphosphatemia, and metabolic acidosis. The severity of these imbalances is proportionate to the degree of renal failure.

34 Physical Assessment Daily weights Fluid intake and output (I&O)
Indicator of fluid status Use same conditions. Fluid intake and output (I&O) 24-hour I&O: compare intake versus output Intake includes all liquids eaten, drunk, or received through IV. Output = Urine, diarrhea, vomitus, gastric suction, wound drainage Laboratory studies Data gathered through a focused physical assessment validate and extend the information collected in the patient history. Daily weights are an important indicator of fluid status. Each kilogram (2.2 lbs) of weight gained or lost overnight is equal to 1 L of fluid retained or lost. These fluid gains or losses indicate changes in the amount of total body fluid, usually ECF, but do not indicate a shift between body compartments. Weigh daily patients with heart failure and those who are at high risk for or who actually have ECV excess. Daily weights are also useful for patients with clinical dehydration or other causes of or risks for ECV deficit. Weigh the patient at the same time each day with the same scale after a patient voids. Calibrate the scale each day or routinely. The patient needs to wear the same clothes or clothes that weigh the same; if using a bed scale, use the same number of sheets on the scale with each weighing. Compare the weight of each day with that of the previous day to determine fluid gains or losses. Look at the weights over several days to recognize trends. Interpretation of daily weights guides medical therapy and nursing care. Teach patients with heart failure to take and record their daily weights at home and to contact their health care provider if their weight increases suddenly by a set amount (obtain parameters from their health care providers). Recognizing trends in daily weights taken at home is important. Research shows that patients who are hospitalized for decompensated heart failure often experience steady increases in daily weights during the week before hospitalization. A weight gain of more than 2.2 lbs (1 kg) was associated with increased risk of hospitalization due to heart failure. Measuring and recording all liquid intake and output (I&O) during a 24-hour period is an important aspect of fluid balance assessment. Compare a patient’s 24-hour intake with his or her 24-hour output. The two measures should be approximately equal if the person has normal fluid balance. To interpret situations in which I&Os are substantially different, consider the individual patient. For example, if intake is substantially greater than output, two possibilities exist: The patient may be gaining excessive fluid or may be returning to normal fluid status by replacing fluid lost previously from the body. Similarly, if intake is substantially smaller than output, two possibilities are known: The patient may be losing needed fluid from the body and developing ECV deficit and/or hypernatremia or may be returning to normal fluid status by excreting excessive fluid gained previously. In most health care settings, I&O measurement is a nursing assessment. Some agencies require a health care provider’s order for I&O. If you want to measure I&O for a patient with compromised fluid status, check your agency policies to determine whether you can institute it or if you need a health care provider’s order. Fluid intake includes all liquids that a person eats (e.g., gelatin, ice cream, soup), drinks, (e.g., water, coffee, juice), or receives through nasogastric or jejunostomy feeding tubes. IV fluids (continuous infusions and intermittent IV piggybacks) and blood components are also sources of intake. Water swallowed while taking pills and liquid medications counts as intake. A patient receiving tube feedings often receives numerous liquid medications, and water is used to flush the tube before and/or after medications. Over a 24-hour period, these liquids amount to significant intake and always are recorded on the I&O record. Ask patients who are alert and oriented to assist with measuring their oral intake, and explain to families why they should not drink or eat from the patient’s meal trays or water pitcher. Fluid output includes urine, diarrhea, vomitus, gastric suction, and drainage from postsurgical wounds or other tubes. Record a patient’s urinary output after each voiding. Instruct patients who are alert, oriented, and ambulatory to save their urine in a calibrated insert, which attaches to the rim of the toilet bowl. Teach patients and families the purpose of I&O measurements. Teach them to notify the nurse or nursing assistive personnel (NAP) to empty any container with voided fluid, or show them how to measure and empty the container themselves and report the results appropriately. Accurate I&O facilitates ongoing evaluation of a patient’s hydration status. Review the patient’s laboratory test results and compare them with normal ranges to obtain further objective data about fluid, electrolyte, and acid-base balances. Serum electrolyte tests usually are performed routinely on any patient entering a hospital to screen for imbalances and serve as a baseline for future comparisons. [Table on text p. 899 covers Focused Nursing Assessments for Patients with Fluid, Electrolyte, and Acid-Base Imbalances.]

35 Case Study (cont’d) Mrs. Reynolds states that she has no appetite, is nauseous, and has been vomiting and has had diarrhea for 7 days. Bowel sounds are hyperactive in all four quadrants. The patient has had only two loose stools since midnight. She voids with difficulty, with dark yellow urine. Her 24-hour intake was 1850 mL; her output was 2200 mL (of which urine was only 1000 mL). Temperature 99.6° F; pulse 100 bpm; BP 110/60 mm Hg with no changes when standing Respirations are 18 breaths per minute and nonlabored with bilateral breath sounds clear to auscultation. Robert observes that Mrs. Reynolds’ skin is dry, and turgor is decreased. Inspection of mucous membranes reveals that they are dry with thick, clear mucus. The patient’s admission weight of 143 lb was down 1 lb since admission. [What conclusions can Robert draw from this information? Discuss.]

36 Measuring Urine Output
These are containers for measuring urine output. Patients need to have good vision and motor skills to perform these measurements. Active involvement of patient and family is an aspect of patient-centered care that is essential for maintaining accurate I&O measurements. When a patient has an indwelling urinary catheter, drainage tube, or suction, record output (e.g., at the end of each nursing shift or every hour) as the patient’s condition requires. You can delegate portions of I&O measurement and recording to NAP with competent skills in measurement. Research shows that visual estimates of fluid volumes often are unreliable; actual measurement is preferable. In many institutions, NAP record oral intake but not intake through feeding or IV tubes, which is a nursing responsibility. Similarly, NAP often record urine, diarrhea, and vomitus output but not drainage through tubes. The responsible registered nurse (RN) or licensed practical nurse/licensed vocational nurse (LPN/LVN) and the NAP work as a team to record measurements in the designated location in the electronic health record (EHR), often on a flow sheet with other information. The EHR program usually calculates 24-hour totals. If an EHR is not used, record I&O on paper forms attached to the bedside chart or room door. You or the NAP can calculate 24-hour totals (see agency policy). [Shown is Figure from text p. 900.]

37 Case Study (cont’d) Mrs. Reynolds’ laboratory results:
Hematocrit 44% (suggesting hypovolemia) Potassium 3.6 mEq/L and sodium 138 mEq/L (both low normal because of prolonged vomiting and diarrhea) Electrocardiogram (ECG) showed normal sinus rhythm. [What nursing diagnosis should Robert choose? Discuss.]

38 Nursing Diagnosis • Decreased cardiac output • Acute confusion
• Impaired gas exchange • Impaired oral mucous membrane • Risk for electrolyte imbalance • Ineffective tissue perfusion • Impaired skin integrity • Deficient fluid volume • Excess fluid volume • Risk for injury • Deficient knowledge regarding disease management Possible nursing diagnoses for patients with fluid, electrolyte, and acid-base alterations are shown on the slide. [Discuss with students how each diagnosis would be determined.] [Box 41-4 on text p. 900 Nursing Diagnostic Process: Deficient Fluid Volume Related to Loss of Gastrointestinal Fluids via Vomiting.]

39 Case Study (cont’d) Nursing diagnosis: Deficient fluid volume related to excessive diarrhea, vomiting, and use of potassium-wasting diuretic Goals: Mrs. Reynolds’ fluid volume will return to normal by time of discharge. Mrs. Reynolds will achieve normal electrolyte balance by discharge. [What expected outcomes would Robert establish for these goals?]

40 Quick Quiz! 3. A senior student nurse delegates the task of intake and output to a new nursing assistant. The student will verify that the nursing assistant understands the task of I&O when the nursing assistant states, A. “I will record the amount of all voided urine.” B. “I will not count liquid stools as output.” C. “I will not record a café mocha as intake.” D. “I will notate perspiration and record it as a small or large amount.” Answer: A

41 Planning Goals and outcomes Setting priorities Collaborative care
Establish an individual patient plan of care that includes mutually established patient goals for each diagnosis. The patient’s clinical condition will determine which diagnoses have the highest priority. If the patient’s medical condition is not dealt with in a timely manner, fluid, electrolyte, and acid-base balances will worsen. For example, if a patient experiences vomiting and diarrhea, this needs to be addressed immediately, especially if the patient is young, elderly, or chronically ill. Do not delegate administration of IV fluid and hemodynamic assessment to NAP. When the patient is stable, you can delegate daily weights, I&O, and direct physical care to NAP. Collaborative care may involve other services, including discharge planning, nutritional support, and pharmacy. Ongoing communication and consultation are important because the patient’s condition can change quickly. [See also Figure on text p. 901 Critical thinking model for fluid, electrolyte, and acid-base balances planning; Nursing Care Plan on pp , Deficient Fluid Volume Related to Increased Output of Gastrointestinal Fluids from Vomiting and Diarrhea; and Concept Map on p. 902.]

42 Case Study (cont’d) Fluid balance Electrolyte and acid-base balance
Urine output will equal intake of ~1500 mL in 2 days. Mucous membranes will be moist in 24 hours. Skin turgor will return to normal within 24 hours. Daily weights will not vary by more than 2 lbs over the next 2 days. Electrolyte and acid-base balance Serum electrolyte and blood counts will be within normal limits within 48 hours. Mrs. Reynolds will not have any nausea or vomiting in 24 hours. [What additional expected outcome would be included? Mrs. Reynolds will not have more than 1 stool a day in 3 days.] [What interventions can you anticipate?]

43 Implementation Health promotion Acute care Fluid replacement education
Teach patients with chronic conditions about risk factors and signs and symptoms of imbalances. Acute care Enteral replacement of fluids Restriction of fluids Parenteral replacement of fluids and electrolytes Total parenteral nutrition Crystalloids (electrolytes) Colloids (blood and blood components) Health promotion activities focus primarily on patient education. Teach patients and caregivers to recognize risk factors for developing imbalances and to implement appropriate preventive measures. Parents must understand that infants and children need to replace fluids when vomiting or diarrhea occurs. Adults, especially the elderly and the infirm, also need to replace fluids when increased perspiration occurs. Patients with chronic health alterations often are at risk for developing fluid, electrolyte, and acid-base imbalances. They need to understand their own risk factors and the measures to be taken to avoid imbalances. Teach patients with chronic diseases and their family caregivers the early signs and symptoms of the fluid, electrolyte, and acid-base imbalances for which they are at risk, and what to do if these occur. Acute care nurses administer medications and oral and IV fluids to replace fluid and electrolyte deficits or to maintain normal homeostasis; they also assist with restricting intake as part of therapy for excesses. •Prevention and treatment of ECV deficit, hypernatremia, and electrolyte deficits are accomplished with enteral or parenteral administration of appropriate fluid. Enteral replacements with oral fluids and electrolytes are indicated for patients who are able to drink. Oral replacements may be contraindicated when the patient is vomiting, has a GI tract obstruction, is at risk for obstruction, or has impaired swallowing. A feeding tube is appropriate when the patient’s GI tract is healthy, but the patient cannot ingest fluids (e.g., after oral surgery, with impaired swallowing). Options for administering fluids include gastrostomy or jejunostomy instillations or infusions through small-bore nasogastric feeding tubes. Patients who have hyponatremia usually require restricted water intake. Patients who have very severe ECV excess sometimes have both sodium and fluid restrictions. It is important to allow patients to choose preferred fluids unless contraindicated. Frequently, patients on fluid restriction can swallow a number of pills with as little as 1 oz (30 mL) of liquid. Parenteral replacement includes total parenteral nutrition (TPN), crystalloids, and colloids (blood and blood components). Total parenteral nutrition (TPN) consists of IV administration of a complex, highly concentrated solution containing nutrients and electrolytes that is formulated to meet a patient’s needs. Depending on their osmolality, PN solutions may be administered through a central IV catheter (high osmolality) or peripherally (lower osmolality).

44 Central Venous Line Central venous lines deliver intravenous fluid into the superior vena cava near the heart. (CVAD, Central venous access device.) IV devices are called peripheral IVs when the catheter tip lies in a vein in one of the extremities; they are called central venous IVs when the catheter tip lies in the central circulatory system (e.g., in the vena cava close to the right atrium of the heart). [Shown is Figure from text p. 905.]

45 IV Therapy IV therapy: crystalloids Types of solutions
Isotonic Hypotonic Hypertonic Caution: Too rapid or excessive infusion of any IV fluid has the potential to cause serious problems Vascular access devices The goal of IV fluid administration is to correct or prevent fluid and electrolyte disturbances. IVs allow direct access to the vascular system, permitting continuous infusion of fluids over a period of time. To provide safe and appropriate therapy to patients who require IV fluids, you need knowledge of the correct ordered solution, the reason the solution was ordered, the equipment needed, the procedures required to initiate an infusion, how to regulate the infusion rate and maintain the system, how to identify and correct problems, and how to discontinue the infusion. [Table on text p. 905 presents types of IV solutions.] An IV solution may be isotonic, hypotonic, or hypertonic. Isotonic solutions have the same effective osmolality as body fluids. Sodium-containing isotonic solutions such as normal saline are indicated for ECV replacement to prevent or treat ECV deficit. Hypotonic solutions have an effective osmolality less than body fluids, thus decreasing osmolality by diluting body fluids and moving water into cells. Hypertonic solutions have an effective osmolality greater than body fluids. If they are hypertonic sodium-containing solutions, they increase osmolality rapidly and pull water out of cells, causing them to shrivel. The decision to use a hypotonic or hypertonic solution is based on the patient’s specific fluid and electrolyte imbalance. Additives such as potassium chloride (KCl) are common in IV solutions. A health care provider’s order is necessary if an IV is to have additives added. Administer KCl carefully because hyperkalemia can cause fatal cardiac dysrhythmias. Under no circumstances should it be administered by IV push (directly through a port in IV tubing). Verify that a patient has adequate kidney function and urine output before administering an IV solution containing potassium. Patients with normal renal function who are receiving nothing by mouth should have potassium added to IV solutions. The body cannot conserve potassium, and the kidneys continue to excrete potassium even when the plasma level falls. Without potassium intake, hypokalemia develops quickly. Vascular access devices (VADs) are catheters or infusion ports designed for repeated access to the vascular system. Peripheral catheters are for short-term use (e.g., fluid restoration after surgery and short-term antibiotic administration). Devices for long-term use include central catheters and implanted ports, which empty into a central vein. Remember that the term central applies to the location of the catheter tip, not to the insertion site. Peripherally inserted central catheters (PICC lines) enter a peripheral arm vein and extend through the venous system to the superior vena cava, where they terminate. Other central lines enter a central vein such as the subclavian or jugular vein or are tunneled through subcutaneous tissue before entering a central vein. Central lines are more effective than peripheral catheters for administering large volumes of fluid, parenteral nutrition (PN), and medications or fluids that irritate veins. Proper care of central line insertion sites is critical for the prevention of catheter-related bloodstream infections (CRBSIs). The National Quality Forum (NQF) identified CRBSIs as one of their endorsed patient safety measures that health care institutions are encouraged to report. Beginning in October of 2008, the Centers for Medicare and Medicaid Services (CMS) no longer reimburses over and above the typical inpatient prospective payment system rate for care required to manage and correct a CRBSI. This means that a hospital is not paid for the added costs and hospital days needed to treat it. Nurses require specialized education regarding care of central venous catheters and implanted infusion ports. Nursing responsibilities for central lines include careful monitoring, flushing to keep the line patent, and site care and dressing changes to prevent CRBSIs.

46 Initiating IV Therapy Equipment Initiating the intravenous line
Vascular access devices (VADs), tourniquets, clean gloves, dressings, IV fluid containers, various types of tubing, and electronic infusion devices (EIDs), also called infusion pumps Initiating the intravenous line Regulating the infusion flow Electronic infusion devices (EIDs or IV pumps) Nonelectronic volume control devices •Initiation and maintenance of IV therapy require clinical decision making, skill, and organized procedures to maintain the sterility and patency of the system. Correct selection and preparation of IV equipment assist in safe and quick placement of an IV line. Because fluids infuse directly into the bloodstream, sterile technique is necessary. The main IV fluid used in a continuous infusion flows through tubing called the primary line. The primary line connects to the IV catheter. Injectable medications such as antibiotics usually are added to a small IV solution bag and “piggybacked” as a secondary set into the primary line, or as a primary intermittent infusion to be administered over a 30- to 60-minute period. The type and amount of solution are prescribed by the patient’s health care provider and depend on the medication added and the patient’s physiological status. After you collect the equipment at the patient’s bedside, prepare to insert the IV line by assessing the patient for a venipuncture site. Venipuncture is a technique in which a vein is punctured through the skin by a sharp rigid stylet. General purposes of venipuncture are to collect a blood specimen, start an IV infusion, provide vascular access for later use, instill a medication, or inject a radiopaque or other tracer for special diagnostic examinations. Nurses require specialized knowledge and education to place peripherally inserted central catheters (PICCs). Some central lines and implanted ports require insertion by physicians or advanced practice nurses. Both types of central catheters require close monitoring and maintenance. This chapter focuses on peripheral catheters. After initiating a peripheral IV infusion and checking it for patency, regulate the rate of infusion according to the health care provider’s orders. Regardless of the method used, nurses are responsible for monitoring fluid flow to prevent overinfusion or underinfusion. Electronic infusion devices (EIDs), also called IV pumps or infusion pumps, deliver an accurate hourly IV infusion rate. Nonelectronic volume control devices are used occasionally with an IV solution infused by gravity to prevent accidental infusion of a large fluid volume.

47 Over-the-Needle Catheter
Shown is an over-the-needle catheter (or peripheral vascular access device) for venipuncture. VADs that are short, peripheral IV catheters are available in a variety of gauges, such as the commonly used 20 and 22 gauges. A larger gauge indicates a smaller-diameter catheter. A peripheral VAD is called an over-the-needle catheter; it consists of a small plastic tube or catheter threaded over a sharp stylet (needle). Once you have inserted the stylet and advanced the catheter into the vein, you withdraw the stylet, leaving the catheter in place. These devices have a safety mechanism that covers the sharp stylet when withdrawing it to reduce the risk of needlestick injury. Needleless systems allow you to make connections without using needles; this reduces needlestick injuries. [Shown is Figure from text p. 906.]

48 Common IV Sites Common IV sites include (A) inner arm and (B) dorsal surface of the hand. Venipuncture is commonly performed in the hand and arm. Remember that the young, elderly, and frail have fragile veins. You will not insert an IV into an area that has signs of infection, infiltration, or thrombosis. Do not use hand veins on older adults or ambulatory patients. IV insertion in a foot vein is common with children, but avoid these sites in adults because of the increased risk of thrombophlebitis. Venipuncture is contraindicated in a site that has signs of infection, infiltration, or thrombosis. An infected site is red, tender, swollen, and possibly warm to the touch. Exudate may be present. Do not use an infected site because of the danger of introducing bacteria from the skin surface into the bloodstream. Avoid using an extremity with a vascular (dialysis) graft/fistula or on the same side as a mastectomy. Avoid areas of flexion if possible. Choose the most distal appropriate site. Using a distal site first allows for the use of proximal sites later if the patient needs a venipuncture site change. [Review Box 41-6 on text p. 907 Focus on Older Adults: Protection of Skin and Veins During Intravenous Therapy.] [Shown is Figure from text p. 906.]

49 Initiating IV Therapy Maintaining the system
Keeping system sterile and intact Changing intravenous fluid containers, tubing, and dressings Assisting patient with self-care activities Complications Fluid overload, infiltration, extravasation, phlebitis, local infection, bleeding at the infusion site Discontinuing peripheral IV access After placing an IV line and regulating the flow rate, maintain the IV system. The frequency and options for maintaining the system are identified in agency policies. An important component of patient care is maintaining the integrity of an IV line to prevent infection. Inserting an IV line under appropriate aseptic technique reduces the chances of contamination from the patient’s skin microflora. After insertion, the conscientious use of infection control principles, including thorough hand hygiene before and after handling any part of the IV system, and maintaining sterility of the system during tubing and fluid container changes, prevents infection. Always maintain the integrity of an IV system. Never disconnect tubing because it becomes tangled, or it might seem more convenient for positioning or moving a patient or applying a gown. If a patient needs more room to maneuver, use aseptic technique to add extension tubing to an IV line. However, keep the use of extension tubing to a minimum because each connection of tubing provides an opportunity for contamination. Never let IV tubing touch the floor. IV tubing contains needleless injection ports through which syringes or other adaptors can be inserted for medication administration. Patients receiving IV therapy over several days require periodic changes of IV fluid containers. It is important to organize tasks so you can change containers rapidly before a thrombus forms in the catheter. Recommended frequency of IV tubing change depends on whether it is used for continuous or intermittent infusion. To prevent the accidental disruption of an IV system, a patient often needs assistance with hygiene, comfort measures, meals, and ambulation. Nurses monitor vigilantly for complications of IV therapy, which include fluid overload, infiltration, phlebitis, local infection, and bleeding at the infusion site. The signs and symptoms of complications often arise rapidly; this highlights the importance of frequent assessment of patients receiving IV therapy. Infiltration occurs when an IV catheter becomes dislodged, or a vein ruptures, and IV fluids inadvertently enter subcutaneous tissue around the venipuncture site. When the IV fluid contains additives that damage tissue, extravasation occurs. Phlebitis (i.e., inflammation of a vein) results from chemical, mechanical, or bacterial causes. Flood volume excess occurs when the fluid is administered too rapidly. Discontinue IV access after infusion of the prescribed amount of fluid; when infiltration, phlebitis, or local infection occurs; or if the IV catheter develops a thrombus at its tip. [See also Box 41-7 on text p. 908 Evidence-Based Practice: Preventing Complications at Peripheral Intravenous Sites; Table on text p. 910 Complications of Intravenous Therapy with Nursing Interventions; Table on text p. 911 Infiltration Scale; and Table on text p. 911 Phlebitis Scale.]

50 Potential Contamination Sites of VADs
These are some potential sites for contamination of a vascular access device. Good IV practice requires periodic updating of procedures based on current research evidence. [Shown is Figure from text p. 908.]

51 Blood Transfusion Blood component therapy = IV administration of whole blood or blood component Blood groups and types Autologous transfusion Transfusing blood Transfusion reactions and other adverse effects Administration of blood or blood products requires a specific procedure for correctly identifying patient and blood products and responding quickly to transfusion reactions. Blood transfusion, or blood component therapy, is the IV administration of whole blood or a blood component such as packed red blood cells (RBCs), platelets, or plasma. Objectives for administering blood transfusions include (1) increasing circulating blood volume after surgery, trauma, or hemorrhage; (2) increasing the number of RBCs and maintaining hemoglobin levels in patients with severe anemia; and (3) providing selected cellular components as replacement therapy (e.g., clotting factors, platelets, albumin). Blood transfusions must be matched to each patient to avoid incompatibility. If incompatible blood is transfused (i.e., a patient’s RBC antigens differ from those transfused), the patient’s antibodies trigger RBC destruction in a potentially dangerous transfusion reaction (i.e., an immune response to the transfused blood components). The most important grouping for transfusion purposes is the ABO system, which identifies A, B, O, and AB blood types. Determination of blood type is based on the presence or absence of A and B red blood cell (RBC) antigens. People with type O blood are considered universal blood donors because they can donate packed RBCs and platelets to people with any ABO blood type. People with type AB blood are called universal blood recipients because they can receive packed RBCs and platelets of any ABO type. Another consideration when matching blood components for transfusions is the Rh factor, which refers to another antigen in RBC membranes. Most people have this antigen and are Rh positive; a person without it is Rh negative. People who are Rh negative receive only Rh-negative blood components. Autologous transfusion (autotransfusion) is the collection and reinfusion of a patient’s own blood. Blood for an autologous transfusion most commonly is obtained by preoperative donation up to 6 weeks before a scheduled surgery. Autologous transfusions are safer for patients because they decrease the risk of mismatched blood and exposure to bloodborne infectious agents. Transfusion of blood or blood components is a nursing procedure that requires an order from a health care provider. A blood transfusion reaction is one of the National Quality Forum’s patient safety measures that should be included in a health care institution’s public reporting of safety events. Patient safety is a nursing priority, and patient assessment, verification of health care provider’s order, and verification of correct blood products for the correct patient are imperative. Perform a thorough patient assessment before initiating a transfusion, and monitor carefully during and after the transfusion. For patient safety, always verify three things: that blood components delivered are the ones that were ordered; that blood delivered to the patient is compatible with the blood type listed in the medical record; and that the right patient receives the blood. Together, two RNs or one RN and an LPN (check agency policy and procedures) must check the label on the blood product against the medical record and against the patient’s identification number, blood group, and complete name. If even a minor discrepancy exists, do not give the blood; notify the blood bank immediately to prevent infusion errors. A transfusion reaction is an immune system reaction to the transfusion that ranges from a mild response to severe anaphylactic shock or acute intravascular hemolysis, both of which are life threatening. Prompt intervention when a transfusion reaction occurs maintains or restores the patient’s physiological stability. When you suspect acute intravascular hemolysis, do the following: Stop the transfusion immediately. Keep the IV line open by replacing the IV tubing down to the catheter hub with new tubing and running 0.9% sodium chloride (normal saline). Do not turn off the blood and simply turn on the 0.9% sodium chloride (normal saline) that is connected to the Y-tubing infusion set. This would cause blood remaining in the IV tubing to infuse into the patient. Even a small amount of mismatched blood can cause a major reaction. Immediately notify the health care provider or emergency response team. Remain with the patient, observing signs and symptoms and monitoring vital signs as often as every 5 minutes. Prepare to administer emergency drugs such as antihistamines, vasopressors, fluids, and corticosteroids per health care provider order or protocol. Prepare to perform cardiopulmonary resuscitation. Save the blood container, tubing, attached labels, and transfusion record for return to the blood bank. Obtain blood and urine specimens per health care provider order or protocol. Circulatory overload is a risk when a patient receives massive whole blood or packed RBC transfusions for massive hemorrhagic shock, or when a patient with normal blood volume receives blood. Transfusion of blood components that are contaminated with bacteria, especially gram-negative bacteria, can cause sepsis. [See also Table on text p. 911 ABO Compatibilities for Transfusion Therapy; Table on text p. 913 Acute Adverse Effects of Transfusions.]

52 Tubing for Transfusions
This photo shows tubing for blood administration. When administering a transfusion, you need an appropriately sized IV catheter and blood administration tubing that has a special in-line filter. Adults require a large catheter (e.g., 18- or 20-gauge) because blood is more viscous than crystalloid IV fluids. Children with small veins use a smaller catheter. Prime the tubing with 0.9% sodium chloride (normal saline) to prevent hemolysis or breakdown of RBCs. Initiate a transfusion slowly to allow for the early detection of a transfusion reaction. Maintain the ordered infusion rate, monitor for side effects, assess vital signs, and promptly record all findings. It is important to stay with the patient during the first 15 minutes—the time when a reaction is most likely to occur. After the initial time period, continue to monitor the patient and obtain vital signs periodically during the transfusion, as directed by agency policy. If a transfusion reaction is anticipated or suspected, obtain vital signs more frequently. The transfusion rate usually is specified in the health care provider’s orders. Ideally, a unit of whole blood or packed RBCs is transfused in 2 hours. This time can be lengthened to 4 hours if the patient is at risk for ECV excess. Beyond 4 hours, risk for bacterial contamination of the blood is present. When patients have severe blood loss, as with hemorrhage, they often receive rapid transfusions through a central venous catheter. A blood-warming device often is necessary because the tip of the central venous catheter lies in the superior vena cava, above the right atrium. Rapid administration of cold blood can cause cardiac dysrhythmias. Patients who receive large-volume transfusion of citrated blood are at high risk for hyperkalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis. [Shown is Figure from text p. 912.]

53 Case Study (cont’d) Administer IV fluids (0.9% normal saline) at 125 mL/hr. Provide patient with an additional 480 mL of noncaffeinated oral fluids every 8 hours. Administer as ordered bismuth subsalicylate (Pepto Bismol) for diarrhea. Maintain accurate I&O measurements. Weigh Mrs. Reynolds daily; monitor trends. Teach Mrs. Reynolds and family about specific dietary modification (potassium-rich foods). Robert will begin teaching regarding the types of foods that offer sources of potassium. [What are the rationales for these interventions? Discuss: Replacement of body fluid restores blood volume and normal serum electrolyte levels; an isotonic solution expands the body’s intravascular fluid volume without causing a fluid shift from one compartment to another. Pepto-Bismol is an antidiarrheal and is given to inhibit GI secretions, stimulate absorption of fluid and electrolytes, inhibit intestinal inflammation, and suppress the growth of Helicobacter pylori. I&O documents hydration and fluid balance for directing therapy. Daily weights provide reliable data on fluid balance. Furosemide (Lasix) is a potassium-wasting diuretic. The body does not store potassium, thus requiring dietary supplements rich in potassium.]

54 Nursing Interventions
Interventions for electrolyte imbalances Support prescribed medical therapies Aim to reverse the existing acid-base imbalance Provide for patient safety Interventions for acid-base imbalances Arterial blood gases In addition to the administration of prescribed medical therapies, nursing interventions may be performed to preserve or restore electrolyte imbalance. Teach patients the reasons for their therapies and the importance of balancing electrolyte I&O to prevent imbalances in the future. Nursing interventions to promote acid-base balance support prescribed medical therapies and aim at reversing the existing acid-base imbalance while providing for patient safety. Patients with acid-base imbalances often require repeated ABG analysis. Determination of a patient’s acid-base status requires obtaining a sample of arterial blood for laboratory testing. An ABG reveals acid-base status and the adequacy of ventilation and oxygenation.

55 Implementation Restorative care Home intravenous therapy
Nutrition support Medication safety Medications OTC drugs Herbal preparations After experiencing acute alterations in fluid, electrolyte, or acid-base balance, patients often require ongoing maintenance to prevent a recurrence of health alterations. Older adults require special considerations to prevent complications from developing. Patient and family teaching is important for preventing fluid, electrolyte, and acid-base imbalances and for effective restorative care. IV therapy often continues in the home setting for patients requiring long-term hydration, PN, or long-term medication administration. A home IV therapy nurse works closely with the patient to ensure that a sterile IV system is maintained, and that complications can be avoided or recognized promptly. [Box 41-8 on text p. 914 summarizes patient education guidelines for home IV therapy.] Most patients who have had electrolyte disorders or metabolic acid-base imbalances require ongoing nutritional support. Depending on the type of disorder, fluid or food intake may be encouraged or restricted. Patients or family members who are responsible for meal preparation need to learn to understand the nutritional content of foods and to read the labels of commercially prepared foods. Numerous medications, OTC drugs, and herbal preparations contain components or create potential side effects that can alter fluid and electrolyte balance. Patients with chronic disease who are receiving multiple medications and those with renal disorders are at significant risk for alterations. Once patients return to a restorative care setting, whether in the home, long-term care, or other setting, drug safety is very important. Patient and family education regarding potential side effects and drug interactions that can alter fluid, electrolyte, or acid-base balance is essential. Review all medications with patients, and encourage them to consult with their local pharmacist, especially if they wish to try a new OTC drug or herbal preparation.

56 Case Study (cont’d) Nursing actions: Findings
Monitor electrolyte levels and daily weights. Inspect oral mucous membranes; assess skin turgor. Evaluate I&O trends during next 48 hours. Findings Serum electrolyte levels: potassium 4.0 mEq/L and sodium 140 mEq/L Mucous membranes remain dry; skin turgor normal Mrs. Reynolds’ 24-hour intake is 2800 mL, and output is 2200 mL with 1800 mL urine. Urine specific gravity is 1.025, and weight has returned to 143 lb. Robert is encouraged by Mrs. Reynolds’ progress. He discusses sources of potassium in the diet and writes this documentation note: “Denies nausea and reports feeling better. No diarrheal stool since yesterday afternoon around 3 pm. On inspection, oral mucosa remains dry, without lesions or inflammation. Skin turgor is normal. Bowel sounds are normal in all four quadrants, abdomen soft to palpation. IV of 0.9% normal saline is infusing in left cephalic vein in forearm at 40 mL/hr per MD order. No tenderness or inflammation at IV site. Is able to identify five food sources for potassium to include in the diet. Is resting comfortably, out of bed in a chair, ate all of breakfast. Will continue to monitor.”

57 Evaluation “What difficulties are you having with measuring your I&O daily and keeping a record?” “What barriers are you experiencing to obtaining the potassium-rich foods you need?” “Are you continuing to have frequent loose stools or diarrhea?” “Have you purchased an antacid, or are you still using baking soda as an antacid?” Evaluation of a patient’s clinical status is especially important if acute fluid, electrolyte, and/or acid-base imbalances exist. A patient’s condition can change very quickly, and it is important to recognize impending problems by integrating information about his or her presenting risk factors and clinical status, effects of the present treatment regimen, and potential causative agent. Some possible questions to ask if expected outcomes have not been met are shown on the slide. [Discuss ways to phrase questions to get honest answers from patients.] [See also Figure Critical thinking model for fluid, electrolyte, and acid-base balances evaluation.]


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