NURS 1060 Electrolyte Imbalances PDF

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This document contains information about electrolyte imbalances. It discusses various aspects of fluid and electrolyte balance with an emphasis on patient care.

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Electrolyte Imbalances NURS 1060: Exam 4 1 OUTCOME u Describe principles of safe, patient-centered, evidence-based nursing care to adults at the basic level, guided by the Caritas philosophy. u Discuss critical thinking and clinical reasoning to provide quality...

Electrolyte Imbalances NURS 1060: Exam 4 1 OUTCOME u Describe principles of safe, patient-centered, evidence-based nursing care to adults at the basic level, guided by the Caritas philosophy. u Discuss critical thinking and clinical reasoning to provide quality patient care. 2 COMPETENCY u Describe factors that create a culture of safety related to medication administration. u Discuss critical thinking and clinical judgment used to provide accurate and safe medication administration. 3 CONCEPT u Fluid and Electrolyte: The physiological mechanisms that maintain fluid and electrolyte balance that promote bodily functions. 4 Unit Outcomes u Describe the nursing process and collaborative management when caring for patients with common fluid and electrolyte imbalances. u Imbalances of Electrolytes: u Sodium u Potassium u Calcium u Phosphorus u Magnesium 5 Labs Contained on a Basic Metabolic Panel (BMP) u Glucose u Calcium u Sodium u Potassium u Bicarbonate (Total CO2) u Chloride u Blood Urea Nitrogen (BUN) u Creatinine Image from Pearson text online Caption: A, Format for a diagram of serum electrolyte results. B, Example that may be seen in a primary care provider’s documentation notes. 6 Sodium Hypernatremia Hyponatremia 7 Sodium 135-145 mEq/L u Imbalances typically associated with parallel changes in osmolality u Plays a major role in u Generation and transmission of nerve impulses u Muscle contractility u The kidneys are the primary regulator of sodium balance. Sodium is the primary determinant of ECF osmolality. (concentration) The serum sodium level reflects the ratio of sodium to water, not necessarily the loss or gain of sodium. Thus, changes in the serum sodium level may reflect a primary water imbalance, a primary sodium imbalance, or a combination of the two. Sodium imbalances are typically associated with ECF imbalances Sodium leaves the body through urine, sweat, and feces. The kidneys are the primary regulator of sodium balance. 8 Hypernatremia Causes u Dehydration u Impaired LOC/inability to obtain fluid. u Diabetes insipidus- body produces too much urine u Excessive sodium intake with inadequate water intake can also lead to Hypernatremia. u ExcessiveIV administration of hypertonic saline (3% Sodium Chloride) also causes cellular dehydration Hypernatremia is not a problem in an alert person who has access to water, can sense thirst, and is able to swallow. Hypernatremia secondary to water deficiency is often the result of an impaired level of consciousness or an inability to obtain fluids. Primary protection is thirst from hypothalamus. A deficiency in the synthesis or release of ADH from the posterior pituitary gland (central diabetes insipidus) or a decrease in kidney responsiveness to ADH (nephrogenic diabetes insipidus) can result in profound diuresis, producing a water deficit and hypernatremia. Hyperosmolality with osmotic diuresis can result from administration of concentrated hyperosmolar tube feedings and hyperglycemia associated with uncontrolled diabetes mellitus. Excessive sweating and increased sensible losses from high fever can also cause hypernatremia. Excessive sodium intake with inadequate water intake can also lead to hypernatremia. Examples of sodium gain include IV administration of hypertonic saline or sodium bicarbonate, use of sodium-containing drugs, excessive oral intake of sodium (ingestion of seawater), and primary aldosteronism. 9 u Signs of Dehydration Hypernatremia u Thirst Symptoms u Dry mucous membranes u Decreased urine output Assessment u Restlessness, Agitation, Lethargy u Muscle twitching Symptomatic hypernatremia is rare. When symptoms do occur, they are primarily the result of water shifting out of cells into the ECT with resultant dehydration and shrinkage of cells, leading to neurologic manifestations. If there is an accompanying ECF volume deficit, manifestations such as postural hypotension, weakness, and decreased skin turgor occur. 10 Treat underlying cause Hypernatremia Primary water deficit—replace fluid orally or IV with isotonic or hypotonic fluids 5% dextrose in water or 0.45% sodium chloride Nursing saline solution. Interventions Excess sodium—dilute with sodium-free IV fluids and promote excretion with diuretics 5% dextrose in water The primary goal of treatment of hypernatremia is to treat the underlying cause. In primary water deficit, fluid replacement is provided either orally or IV with isotonic or hypotonic fluids such as 5% dextrose in water or 0.45% sodium chloride saline solution. If sodium excess, dilute the sodium concentration with sodium-free IV fluids, such as 5% dextrose in water, and promote excretion of the excess sodium by administering diuretics. Monitor serum sodium levels and the patient’s response to therapy. Quickly reducing serum sodium levels can cause a rapid shift of water back into the cells, resulting in cerebral edema and neurologic complications. This risk is greatest in the patient who has developed hypernatremia over several days or longer. 11 u Monitor serum sodium levels Hypernatremia u Monitor neuro u Quickly reducing serum sodium levels Nursing can cause a rapid shift of water back into the cells Interventions u May result in cerebral edema and neurologic complications- seizures The most serious complication of hypernatremia is subarachnoid or subdural hemorrhage due to the rupture of bridging veins and dural sinus thrombosis. It can lead to permanent brain damage or death. Rapid correction of chronic hypernatremia causes cerebral edema, seizure, and permanent brain damage. https://www.ncbi.nlm.nih.gov/books/NBK441960/ 12 Case Study Hyponatremia u M.H., a 62-year-old female, was admitted with confusion and lethargy related to hyponatremia (126 mEq/L). u Her husband tells you that M.H. had diarrhea over the past week and was drinking lots of water to prevent dehydration. u What caused M.H.’s serum sodium level to fall? Excessive diarrhea can cause fluid and sodium loss. Replacing fluid with plain water can lead to a dilutional hyponatremia. In other words, sodium loss is greater than net water loss. 13 u Excessive diarrhea can cause fluid and sodium loss. u Replacing fluid with plain water Case Study can lead to a dilution hyponatremia Hyponatremia u Sodium loss is greater than net water loss 14 Hyponatremia Common Causes Loss of sodium-rich body fluids Excess Fluid Intake Diuretics, renal disease, profuse inappropriate use of sodium-free or diaphoresis, draining wounds, excessive hypotonic IV fluids. This may occur in diarrhea or vomiting, trauma with patients after surgery. significant blood loss 15 Hyponatremia u Confusion, headache Symptoms u Nausea Assessment u Seizures (severe cases) 16 u As you admit M.H. to the nursing unit, you develop an Case Study individualized plan of care. Hyponatremia u What are priority nursing interventions for M.H.? 17 Hyponatremia Nursing Interventions u Fluid restriction u If caused by water excess u Sodium replacement u May have orders for small amount of IV hypertonic saline solution (3% NaCl) u Monitor neuro status Severe symptoms (seizures) u Room assignment where they will be central to the unit to monitor and prevent falls (Acute confusion, Risk for Falls/Injury) In hyponatremia caused by water excess, fluid restriction is often the only treatment. If severe symptoms (seizures) develop, small amounts of IV hypertonic saline solution (3% NaCl) can restore the serum sodium level while the body is returning to a normal water balance. 18 Potassium Hyperkalemia Hypokalemia 19 Potassium Major ICF cation (3.5 – 5.3 Necessary for: mEq/L) Critical values 7.0 mEq/L or higher Transmission and conduction of nerve and Critical values 2.5 mEq/L or less muscle impulses Cellular growth Maintenance of cardiac rhythms Potassium is the major ICF cation, with 98% of the body potassium being intracellular. For example, potassium concentration within muscle cells is approximately 140 mEq/L; potassium concentration in the ECF is 3.5 to 5.0 mEq/L. The sodium-potassium pump in cell membranes maintains this concentration difference by pumping potassium into the cell and sodium out. The ratio of ECF to ICF potassium is the major factor in the resting membrane potential of nerve and muscle cells. Neuromuscular and cardiac function are commonly affected by potassium imbalances. Potassium is required for glycogen to be deposited in muscle and liver cells. Potassium also plays a role in acid-base balance. 20 Potassium u The sodium-potassium pump in cell membranes pumps u potassium IN u sodium out u The ratio of ECF to ICF potassium is the major factor in the resting membrane potential of nerve and muscle cells. u Neuromuscular and cardiac function are commonly affected by potassium imbalances. u Potassium is required for glycogen to be deposited in muscle and liver cells. K+glucose+insulin 21 u Fruits and vegetables (bananas and oranges) u Salt substitutes u saltsubstitutes contain approximately Sources of 50–60 mEq of potassium per teaspoon Potassium and raise potassium u Potassium medications (PO, IV) u Stored blood Diet is the source of potassium. The typical Western diet contains approximately 50 to 100 mEq of potassium daily, mainly from fruits, dried fruits, and vegetables. Many salt substitutes used in low-sodium diets contain substantial potassium. Patients may receive potassium from parenteral sources, including IV fluids; transfusions of stored, hemolyzed blood; and medications (e.g., potassium penicillin). The kidneys are the primary route for potassium loss, eliminating about 90% of the daily potassium intake. The remainder is lost in the stool and sweat. There is an inverse relationship between sodium and potassium reabsorption in the kidneys. Factors that cause sodium retention (e.g., low blood volume, increased aldosterone level) cause potassium loss in the urine. Large urine volumes can be associated with excess loss of potassium in the urine. If kidney function is significantly impaired, retained potassium can lead to toxic levels. 22 Potassium u Regulated by kidneys u There is an inverse relationship between sodium and potassium reabsorption in the kidneys. u Factors that cause sodium retention (e.g., low blood volume, increased aldosterone level) cause potassium loss in the urine. u If kidney function is significantly impaired, retained potassium can lead to toxic levels. 23 Hyperkalemia Causes u Renal Failure u Medications u ACE inhibitors u Potassium-sparing diuretics u Acidosis u Cell destruction (hemolysis, burns, trauma) 24 Hyperkalemia (High Potassium) u Hyperkalemia increases the concentration of potassium outside of the cell, altering the normal ECF and ICF ratio, resulting in increased cellular excitability. Hyperkalemia increases the concentration of potassium outside of the cell, altering the normal ECF and ICF ratio, resulting in increased cellular excitability. Initially as the levels of potassium increase, the patient may experience cramping leg pain and weakness, followed by weakness or paralysis of other skeletal muscles, including the respiratory muscles. Abdominal cramping and diarrhea occur from hyperactivity of smooth muscles. (See next slide for discussion of cardiac dysrhythmias.) 25 Hyperkalemia Symptoms Assessment Muscle cramps and numbness (weakness, respiratory distress, abdominal cramping) Cardiac Rhythm (ECG) Changes *peaked T wave Nursing Diagnoses associated: Risk for activity intolerance The patient with hyperkalemia is at risk for activity intolerance and injury related to lower extremity muscle weakness. Risk for electrolyte imbalance Risk for injury Potential complication: dysrhythmias 26 ECG Effects of Hyperkalemia The most clinically significant manifestations of hyperkalemia are the disturbances in cardiac conduction. Peaked T wave Cardiac depolarization is decreased, leading to flattening of the P wave and widening of the QRS complex. Repolarization occurs more rapidly, resulting in shortening of the QT interval and causing the T wave to be narrower and more peaked. Ventricular fibrillation or cardiac standstill may occur. 27 Hyperkalemia Nursing Interventions u Decrease oral and parenteral K intake u Increase elimination of K u Loop Diuretics u Dialysis u Kayexalate When the elevation of potassium is mild and the kidneys are functioning, it may be sufficient to withhold potassium from the diet and IV sources and increase renal elimination by administering fluids and possibly diuretics. Kayexalate, administered orally or rectally, binds potassium in exchange for sodium and the resin is excreted in feces. 28 Hyperkalemia- Moderate/Severe Nursing Interventions u IV insulin and dextrose (Potassium will be forced to enter cell via Na-K pump) u IV Calcium gluconate or calcium chloride u IV Sodium Bicarbonate (for acidosis) All patients with clinically significant hyperkalemia should be monitored electrocardiographically to detect dysrhythmias. Patients with moderate hyperkalemia should additionally receive one of the treatments to force potassium into cells—usually IV insulin and glucose. Sodium bicarbonate is used if the patient is acidotic. All patients with clinically significant hyperkalemia should be monitored electrocardiographically to detect dysrhythmias and to monitor the effects of therapy. The patient experiencing dangerous cardiac dysrhythmias should receive IV calcium gluconate immediately. Monitor blood pressure because rapid administration of calcium can cause hypotension. 29 Hypokalemia (Low Potassium) Caused by: Increased loss of K+ via the Renal losses occur when the patient has a low magnesium level kidneys or is taking diuretics Increased loss of K+ via the GI tract losses of potassium are associated with diarrhea, laxative gastrointestinal tract abuse, vomiting The most common causes of hypokalemia are abnormal losses from either the kidneys or the GI tract. GI tract losses of potassium are associated with diarrhea, laxative abuse, vomiting, and ileostomy drainage. Renal losses occur when the patient has a low magnesium level or is diuresing, particularly in the patient with an elevated aldosterone level. Aldosterone is released when the circulating blood volume is low; causing sodium retention in the kidneys with a loss of potassium in the urine. Low plasma magnesium stimulates renin release and subsequent increased aldosterone levels, which results in potassium excretion. Factors causing potassium to move from the ECF to the ICF are insulin therapy (especially in conjunction with diabetic ketoacidosis) and β-adrenergic stimulation (catecholamine release in stress, coronary ischemia, delirium tremens, administration of β-adrenergic agonist drugs). Alkalosis can cause a shift of potassium into cells in exchange for hydrogen, thus lowering the potassium in the ECF and causing symptomatic hypokalemia. 30 Case Study: Fluid and Electrolyte Imbalances u T.M., a 76-year-old male, is brought to emergency department with confusion and lethargy. u He has a history of hypertension and type 2 diabetes. u Patient doubled his furosemide (Lasix) dose for the last 2 weeks because he felt “puffy.”. 31 Case Study: Fluid and Electrolyte Imbalances u T.M.’s lab results include serum K+ 2.8 and Hct 66%. u What is the probable cause of T.M.’s hypokalemia? u Explain the Hct lab result based on T.M.’s recent history. u For what clinical manifestations would you assess T.M.? T.M.’s doubling of his Lasix dosage has resulted in increased diuresis and subsequent increased renal excretion of water and potassium. The Hct level is elevated secondary to ECF fluid loss. Hct = 39-47% Female Hct = 44-52% Male Clinical manifestations are explained on next slide. 32 Case Study: Fluid and Electrolyte Imbalances u T.M.ʼs doubling of his Lasix dosage has resulted in increased diuresis and subsequent increased renal excretion of water and potassium. u The Hct level is elevated secondary to ECF fluid loss. u Hct = 39-47% Female u Hct = 44-52% Male u Hctis concentrated in less fluid so the value appears increased 33 Cardiac Dysrhythmias *most serious Skeletal muscle weakness (legs), Lethargy Hypokalemia Symptoms Weakness of respiratory muscles (low RR, shallow) Assessment Polyuria Hyperglycemia Hypokalemia alters the resting membrane potential, resulting in hyperpolarization (an increahypokalemia involve changes in cardiac and muscle function. sed negative charge within the cell) and impaired muscle contraction. Therefore, the manifestations of Skeletal muscle weakness and paralysis may occur with hypokalemia. As with hyperkalemia, hypokalemia initially affects leg muscles. Severe hypokalemia can cause weakness or paralysis of respiratory muscles, leading to shallow respirations and respiratory arrest. Alterations in smooth muscle function may lead to decreased GI motility (e.g., paralytic ileus), decreased airway responsiveness, and impaired regulation of arteriolar blood flow, possibly contributing to smooth muscle cell breakdown. Finally, hypokalemia can impair function in nonmuscle tissue by impairing insulin secretion, leading to hyperglycemia. 34 Case Study: Fluid and Electrolyte Imbalances u Assessment of T.M. reveals the following: u Poor skin turgor, c/o leg cramps, lethargy u Heart rate 135 and irregular u Respiratory rate 26 u BP 110/58 Nursing diagnoses for hypokalemia: Risk for activity intolerance Risk for electrolyte imbalance Risk for injury Based on Assessment: Is one is missing? Potential complication: Dysrhythmias The patient with hyperkalemia is at risk for activity intolerance and injury related to muscle weakness and hyporeflexia. The patient is also at increased risk for cardiac dysrhythmias. T.M.’s fluid volume deficit also places him at increased risk for injury and activity intolerance related to postural hypotension and decreased cardiac output. 35 Case Study: Fluid and Electrolyte Imbalances u T.M. is started on 0.45 % NaCl and potassium chloride replacement is ordered. u How will you administer the potassium chloride? u What are your priority nursing interventions? 36 Hypokalemia Nursing Interventions u Dietary intake- increase potassium u KCl supplements PO u KCl supplements IV u NEVER give KCL via IV push or as a bolus. u Shouldalways be a diluted form and not exceed 10-20 mEq/hr to prevent hyperkalemia and cardiac arrest KCl is not given unless there is urine output of at least 30 mL/hour IV KCl must always be diluted and never given in concentrated amounts. If a larger concentration or rate is necessary: MANDATORY FOR continuous cardiac monitoring. The rate of IV administration of KCl should not exceed 10 to 20 mEq per hour and must be administered by infusion pump to ensure correct administration rate. The preferred maximum concentration is 40 mEq/L. However, stronger concentrations may be given for severe hypokalemia (up to 80 mEq/L) with continuous cardiac monitoring. Because KCl is irritating to the vein, assess IV sites at least hourly for phlebitis and infiltration. Infiltration can cause necrosis and sloughing of the surrounding tissue. Use a central IV line when rapid correction of hypokalemia is necessary. Patients at risk for hypokalemia and those who are critically ill should have cardiac monitoring to detect cardiac changes related to potassium imbalances. 37 Case Study: Fluid and Electrolyte Imbalances u T.M.’s serum electrolytes and fluid volume status return to normal. u What important teaching should be done with T.M. in anticipation of discharge? Teach the patient the signs and symptoms of hypokalemia and to report their appearance to the health care provider. Explain the importance of increasing dietary potassium intake when taking Lasix. Teach patients about foods high in potassium. Explain that salt substitutes contain approximately 50–60 mEq of potassium per teaspoon and help raise potassium if taking a potassium-losing diuretic. Emphasize the importance of taking his medication as prescribed, and teach him that there are serious consequences if he takes his medication incorrectly. Emphasize the importance of consulting with MD before changing his medication. 38 Case Study Fluid and Electrolyte Teaching for Safe Discharge Preparation u Importance of increasing dietary potassium when taking loop diuretics (furosemide) u Foods high in potassium u Importance of taking medication as prescribed and possible consequences if taken incorrectly u Symptoms of hypokalemia and fluid imbalances u Consult with MD before changing his medication 39 Calcium Hypercalcemia Hypocalcemia 40 Formation of teeth and bone Blood clotting Calcium (8.5-10.5 Transmission of nerve impulses mg/dl) Myocardial contractions Muscle contractions Calcium is necessary for many metabolic processes. It is the major cation in the structure of bones and teeth. Other functions of calcium include blood-clotting, transmission of nerve impulses, myocardial contractions, and muscle contractions. 41 Calcium Sources u Obtained from ingested foods u Dairy, green leafy vegetables, beans u Need vitamin D to absorb calcium u Vitamin D is either ingested in the diet or formed in the skin in the presence of sunlight The source of calcium is dietary intake. Calcium absorption requires the active form of vitamin D. Vitamin D is either ingested in the diet or formed in the skin in the presence of sunlight. Calcium is present in the serum in three forms: free or ionized; bound to protein (primarily albumin); and complexed with phosphate, citrate, or carbonate. Total serum calcium levels reflect the total calcium level (all three forms), although ionized calcium levels may be analyzed and reported separately. Changes in serum pH will alter the level of ionized calcium without altering the total calcium level. A decreased plasma pH (acidosis) decreases calcium binding to albumin, leading to more ionized calcium. An increased plasma pH (alkalosis) increases calcium binding, leading to decreased ionized calcium. Alterations in serum albumin levels affect the interpretation of total calcium levels. Low albumin levels result in a drop in the total calcium level, although the level of ionized calcium is not affected. 42 Calcium- balance controlled by Parathyroid hormone and Calcitonin u Parathyroid hormone u Produced by the parathyroid gland-production and release are stimulated by low serum calcium levels u Raises the level of serum calcium u Increases movement of calcium out of bones, increases GI absorption of calcium, and increases renal tubule reabsorption of calcium. u Calcitonin u Produced by the thyroid gland- stimulated by high serum calcium levels u Lowers the level of serum calcium u Decreasing GI absorption, increasing calcium deposition into bone, and promoting renal excretion PTH is produced by the parathyroid gland. Its production and release are stimulated by low serum calcium levels. PTH increases bone resorption (movement of calcium out of bones), increases GI absorption of calcium, and increases renal tubule reabsorption of calcium. Calcitonin is produced by the thyroid gland and is stimulated by high serum calcium levels. It opposes the action of PTH and lowers the level of serum calcium by decreasing GI absorption, increasing calcium deposition into bone, and promoting renal excretion. Image Retrieved from https://www.google.com/search?q=thyroid+parathyroid&rlz=1C1GCEU_enU S821US822&sxsrf=AOaemvJzQfsfCdMLghk_XtgOAqqtDFv20Q:163767440 0448&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjup5XHzK70AhVmkmo FHYoJB84Q_AUoAnoECAEQBA&biw=1536&bih=722&dpr=1.25#imgrc=vktt W9IBsJGwgM 43 u Hyperparathyroidism (two thirds of cases) Hypercalcemia u Malignancy Causes u Prolonged immobilization u resultsin bone mineral loss and increased plasma calcium concentration Hypercalcemia is caused by hyperparathyroidism in about two thirds of the cases. Malignancy, especially from myeloma and breast, lung, and kidney cancers, causes the remaining third. Malignancies lead to hypercalcemia through bone destruction from tumor invasion or through tumor secretion of a parathyroid-related protein, which stimulates calcium release from bones. Hypercalcemia is also associated with prolonged immobilization, which results in bone mineral loss and increased plasma calcium concentration. More rare causes include vitamin D overdose or increased calcium intake (e.g., ingestion of antacids containing calcium, excessive administration during cardiac arrest). 44 Hypercalcemia Symptoms Assessment u Lethargy, muscle weakness, confusion, decreased reflexes u From decreased excitability of muscle and nerve cells u Constipation u Bone pain, fractures u Kidney stones Excess calcium leads to reduced excitability of both muscles and nerves. 45 u Loop diuretics- promote excretion Hypercalcemia u Hydrating with isotonic saline IV u PO Fluid 3000 to 4000 mL daily to Nursing promote the renal excretion of Interventions calcium and decrease kidney stone formation 46 u Diet low in calcium (Vitamins) u Increase in weight-bearing activity to enhance bone mineralization. Hypercalcemia u Synthetic Calcitonin given IM or subcutaneously lowers serum calcium levels. Nursing u Bisphosphonates (example: Fosamax) Interventions u Most effective agents in treating hypercalcemia and osteoporosis u Medication inhibits the activity of osteoclasts (cells that break down bone and result in calcium release) 47 Hypocalcemia Possible Causes u Parathyroid hormone deficiency u Vitamin D deficiency u Chronic Kidney Disease u Malabsorption u Overuse of laxatives u Disease such as Crohns or Celiacs Acute pancreatitis Lipolysis, a consequence of pancreatitis, produces fatty acids that combine with calcium ions, decreasing serum calcium levels. Multiple blood transfusions citrate used to anticoagulate the blood- binds with the calcium 48 u Tetany u Positive Trousseau’s or Chvostek’s Hypocalcemia sign Symptoms u Laryngeal stridor, Dysphagia, Tingling around the mouth or in the Assessment extremities u Cardiac dysrhythmias- prolonged QT interval Low levels of calcium allow sodium to move into excitable cells, decreasing the threshold of action potentials with subsequent depolarization of the cells. This results in increased nerve excitability and sustained muscle contraction (tetany). A positive Trousseau’s or Chovostek’s sign is indicative of hyperreflexia noted with hypercalcemia. {See next slide for figure about testing for hypocalcemia.} A. Chvostek’s sign is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear. B. Trousseau’s sign is a carpal spasm induced by inflating a blood pressure cuff above the systolic pressure for a few minutes. Excess neuromuscular excitability causes other clinical manifestations, including stridor, dysphagia, tingling around mouth or in extremities Cardiac effects of hypocalcemia include decreased cardiac contractility and ECG changes. A prolonged QT interval may develop into a ventricular tachycardia. 49 Tests for Hypocalcemia A. Chvostek'sʼs sign is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear. B and C. Trousseauʼs sign is a carpal spasm induced by inflating a blood pressure cuff above the systolic pressure for a few minutes. A. Chvostek’s sign is contraction of facial muscles in response to a light tap over the facial nerve in front of the ear. B. Trousseau’s sign is a carpal spasm induced by inflating a blood pressure cuff above the systolic pressure for a few minutes. Chvostek's sign (Figure 1A and Video 1) and Trousseau's sign (Figure 1B and Video 2), a result of postsurgical acquired hypoparathyroidism. 50 Hypocalcemia- Mild Nursing Implementation u Diet high in calcium-rich foods and vitamin D supplementation. u Oral calcium supplements, such as calcium carbonate or citrate, can be used when patients are unable to consume enough dietary calcium, such as those who do not tolerate dairy products. 51 Hypocalcemia- Severe Nursing Interventions u IV preparations of calcium (e.g., calcium gluconate, calcium chloride) are given. u Not IM to avoid local reactions u Assess for laryngeal spasms, swallowing u Seizure precautions 52 Phosphate Hyperphosphatemia Hypophosphatemia 53 Phosphate (2.5 - 4.5 mg/dl) u Stored in the bones and teeth as calcium phosphate u Serum levels controlled by parathyroid hormone (PTH) u Essential to function of muscle, red blood cells, and nervous system u Involved in acid-base buffering system, ATP production, cellular uptake of glucose, and metabolism of carbohydrates, proteins, and fats Phosphate is the primary anion in the ICF and the second most abundant element in the body, second to calcium. Most phosphorus is in the bones and teeth as calcium phosphate. The remaining phosphorus is metabolically active and essential to the function of muscle, RBCs, and the nervous system. It is also involved in the acid-base buffering system, the mitochondrial formation of ATP, cellular uptake and use of glucose, and the metabolism of carbohydrates, proteins, and fats. Phosphate PO4(3-) Phosphorous P 54 Phosphate u Maintenance requires adequate renal functioning u Kidneys are the major route of phosphate excretion. u When the phosphate level in the glomerular filtrate falls below the normal level or PTH levels are low, the kidneys reabsorb additional phosphorus. 55 Phosphate u A reciprocal relationship exists between phosphorus and calcium u High serum phosphate level tends to cause a low calcium concentration in the serum. u Low serum calcium levels stimulate the release of PTH, which decreases reabsorption of phosphorus 56 Hyperphosphatemia u Rare and often asymptomatic u hypocalcemia symptoms possible- neuromuscular irritability and tetany u Ca ¯ P­ u Can be caused by excessive intake Mild hyperphosphatemia is often asymptomatic. The clinical manifestations of more severe hyperphosphatemia primarily relate to the low serum calcium levels often associated with high serum phosphate levels. These include tetany, muscle cramps, paresthesias, and seizures. Increased levels of phosphate readily precipitate with calcium, and calcified deposits occur outside of the bones. These metastatic calcium precipitates can be found in soft tissues such as joints, arteries, skin, kidneys, and corneas and produce organ dysfunction, notably renal failure. 57 Hyperphosphatemia Nursing Management Restrict foods and fluids dairy products containing phosphorus calcium carbonate limits intestinal phosphate absorption and increase Phosphate-binding agents phosphate secretion into the intestine. Adequate hydration and hydration and increasing calcium correction of hypocalcemic levels assist with returning conditions phosphorus levels to normal. The primary management of hyperphosphatemia is identifying and treating the underlying cause. Ingestion of foods and fluids high in phosphorus (e.g., dairy products) should be restricted. Phosphate-binding agents or gels (e.g., calcium carbonate) limit intestinal phosphate absorption and increase phosphate secretion into the intestine. If hypocalcemia is present, adequate hydration and instituting measures to correct calcium levels assist with returning phosphorus levels to normal. With severe hyperphosphatemia, hemodialysis or an insulin and glucose infusion can rapidly decrease levels. 58 Clinical Application u Parathyroid hormone (PTH) regulates calcium concentration u Acute hypoparathyroidism (low PTH) causes u low plasma calcium (tetany) u high plasma phosphate level u Hypoparathyroid tetany is treated with IV calcium gluconate 59 u Malnourishment/ malabsorption (low Hypophosphatemia vitamin D) u Alcoholism Causes u Use of phosphate-binding antacids Hypophosphatemia is rare but may occur in the patient who is malnourished or has a malabsorption syndrome. Other causes include alcohol withdrawal and use of phosphate-binding antacids. Hypophosphatemia may also occur during parenteral nutrition with inadequate phosphorus replacement. 60 Hypophosphatemia Symptoms Assessment u Mild often asymptomatic u Severe can impact cellular function (CNS depression, confusion, muscle weakness) Most clinical manifestations of hypophosphatemia result from impaired cellular energy and oxygen delivery related to deficient cellular ATP and 2,3- diphosphoglycerate (2,3-DPG), an enzyme in RBCs that facilitates oxygen delivery to the tissues. Mild to moderate hypophosphatemia is often asymptomatic. Severe hypophosphatemia may be fatal because of decreased cellular function. Acute manifestations include CNS depression, confusion, and other mental changes. Other manifestations include muscle weakness and pain, dysrhythmias, and cardiomyopathy. Results from impaired cellular energy and oxygen delivery related to deficient cellular ATP and an enzyme (requires P) in RBCs that facilitates oxygen delivery to the tissues. 61 u Oral supplementation u Neutra-Phos u Dietary increase Hypophosphatemia phosphorus u dairy products Interventions u IV administration of potassium phosphate Management of a mild phosphorus deficiency may involve oral supplementation (e.g., Neutra-Phos) and ingestion of foods high in phosphorus (e.g., dairy products). Symptomatic hypophosphatemia can be fatal and often requires IV administration of sodium phosphate or potassium phosphate. Frequent monitoring of serum phosphate and calcium levels is necessary to guide IV therapy. Sudden symptomatic hypocalcemia, secondary to increased calcium phosphorus binding, is a potential complication of IV phosphorus administration. 62 Magnesium Hypermagnesemia Hypomagnesemia 63 Magnesium (1.5 – 2.5 mEq/L) u Essential cellular processes u Coenzyme in metabolism of protein and carbohydrates u Required for nucleic acid and protein synthesis u Helps maintain calcium and potassium balance u Necessary for sodium-potassium pump Magnesium is the second most abundant intracellular cation. Magnesium plays an important role in many essential cellular processes. The most notable is the activation of a wide variety of enzyme systems. Magnesium is a coenzyme in the metabolism of carbohydrates and protein and is required for the synthesis of nucleic acids and proteins. Magnesium plays a role in maintaining normal calcium and potassium balance. Manifestations of magnesium imbalance are often mistaken for calcium imbalances. Because magnesium, calcium, and potassium balance are closely related, assess all three cations together. Adequate intracellular magnesium is necessary for normal function of the sodium- potassium pump. 64 Magnesium u Acts directly on affect neuromuscular excitability u Important for normal cardiac function u Contained in bone u Magnesium is regulated by GI absorption and renal excretion. Because magnesium acts directly on the myoneural junction, alterations in serum magnesium levels profoundly affect neuromuscular excitability and contractility, including cardiac function. Approximately 50% to 60% of the body’s magnesium is contained in bone. Only a small amount (2%) is in the ECF, with the remainder inside the cell. Magnesium is regulated by GI absorption and renal excretion. The kidneys are able to conserve magnesium in times of need and excrete excesses. Factors that regulate calcium balance (e.g., PTH) similarly influence magnesium balance. 65 Medications- Maalox, milk of magnesium containing magnesia antacids Hypermagnesemia Causes Impaired Renal function Hypermagnesemia usually occurs only with an increase in magnesium intake accompanied by renal insufficiency or failure. A patient with chronic kidney disease who ingests products containing magnesium (e.g., Maalox, milk of magnesia) will have a problem with excess magnesium. Magnesium excess could develop in the pregnant woman who receives magnesium sulfate for the management of eclampsia. 66 Depressed Neuromuscular and CNS functions Hypermagnesemia Symptoms u Lethargy u Flaccid muscle tone Assessment u Decreased reflexes Hypermagnesemia depresses neuromuscular and CNS functions. Initial clinical manifestations of a mildly elevated serum magnesium concentration include lethargy, nausea, and vomiting. As the levels of serum magnesium increase, deep tendon reflexes are lost, followed by somnolence, and then respiratory and, ultimately, cardiac arrest can occur. 67 Hypermagnesemia Clinical Management u Emergency treatment u IV Calcium Gluconate u Diuretics or dialysis u Patients with kidney disease should not take magnesium-containing drugs, and ingestion of magnesium containing foods (e.g., green vegetables, nuts, bananas, oranges, peanut butter, chocolate). Management of hypermagnesemia should focus on prevention. Persons with chronic kidney disease should not take magnesium-containing drugs, and ingestion of magnesium containing foods (e.g., green vegetables, nuts, bananas, oranges, peanut butter, chocolate) should be restricted. The emergency treatment of hypermagnesemia is IV administration of calcium chloride or calcium gluconate to oppose the effects of the magnesium on cardiac muscle. If renal function is adequate, promoting urinary excretion with oral and parenteral fluids and IV furosemide (Lasix) decreases magnesium levels. The patient with impaired renal function will require dialysis because the kidneys are the major route of excretion for magnesium. 68 Hypomagnesemia Causes u Poor dietary intake u Chronic alcoholism u Starvation u Diuretics increase the risk of magnesium loss through renal excretion. Hypomagnesemia occurs in patients with limited magnesium intake or increased renal losses. Major causes of hypomagnesemia from insufficient food intake include prolonged fasting or starvation and chronic alcoholism. Fluid loss from the GI tract interferes with magnesium absorption. Another potential cause of hypomagnesemia is prolonged parenteral nutrition without magnesium supplementation. Many diuretics increase the risk of magnesium loss through renal excretion. In addition, osmotic diuresis caused by high glucose levels in uncontrolled diabetes mellitus increases renal excretion of magnesium. 69 Hypomagnesemia Symptoms Assessment Neuromuscular and CNS hyperexcitability u Confusion u Hyperactive reflexes u Muscle cramps, tremors u Cardiac dysrhythmias u Positive Chvostek’s sign Hypomagnesemia produces neuromuscular and CNS hyperirritability. Clinical manifestations include confusion, hyperactive deep tendon reflexes, muscle cramps, tremors, and seizures. Magnesium deficiency also predisposes to cardiac dysrhythmias, such as premature ventricular contractions and ventricular fibrillation. Clinically, hypomagnesemia resembles hypocalcemia and may contribute to the development of hypocalcemia resulting from the decreased action of PTH. Hypomagnesemia may also be associated with hypokalemia that does not respond well to potassium replacement. This occurs because intracellular magnesium is critical to normal function of the sodium-potassium pump. 70 Hypomagnesemia Interventions u Oral supplements u Increase dietary intake u green vegetables, nuts, bananas, oranges, peanut butter, and chocolate u Parenteral IV or IM magnesium when severe u When Magnesium sulfate is given: u Monitor vital signs u Use an infusion pump- too rapid administration of magnesium can lead to cardiac or respiratory arrest. The primary goal of treatment of hypomagnesemia is to treat the underlying cause. Management of mild magnesium deficiencies involves oral supplements and increased dietary intake of foods high in magnesium (green vegetables, nuts, bananas, oranges, peanut butter, and chocolate). If hypomagnesemia is severe or if hypocalcemia is present, IV magnesium (e.g., magnesium sulfate) is given. Monitor vital signs and use an infusion pump as too rapid administration of magnesium can lead to cardiac or respiratory arrest. 71

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