Fluids and Electrolytes 2024 PDF

 FLUIDS vital in all forms of life help maintain body temperature and cell shape, and they help transport nutrients, gases, and wastes What will happen if we lose fluid in the body? Loading… Factors influencing the amount of bo...

 FLUIDS vital in all forms of life help maintain body temperature and cell shape, and they help transport nutrients, gases, and wastes What will happen if we lose fluid in the body? Loading… Factors influencing the amount of body fluids Age Gender Body fat  BODY FLUIDS Provides transportation of nutrients to the cells and carries waste products from the cells Loading… total body fluid amounts to about 60% of body weight a loss of 10% of body fluid in the adult is serious a loss of 20% of the body fluid content in the adult is serious  CONSTITUENT OF BODY FLUIDS body fluids consist of water and dissolved substances the largest single fluid constituent of the body is water some substances such as GLUCOSE, UREA, and CREATININE do not dissociate in solution, that is, they do not separate from their complex form into simpler substances they are in solution Amount and composition of body fluids water and electrolytes Fluid compartments COMPARTMENTS ICF (within the cell): Contains the necessary nutrients and electrolytes (potassium = K, magnesium = Mg, phosphate = Ph, and chloride = Cl) required to provide cell maintenance and remove wastes Extracellular fluid (ECF) (ISF [around the cell]) and IVF (within the blood vessels): Contain electrolytes (sodium = Na, calcium = Ca, and chloride = Cl)  COMPOSITION OF ECF INTRAVASCULAR Fluid within the blood vessel that contains plasma INTERSTITIAL Fluid that surrounds the cell TRANSCELLULAR Smallest division of ECF Fluid that fills up the spaces of chambers that are created or formed from the linings of epithelial cells  MECHANISMS OF FLUID LOSS INSENSIBLE LOSS Can’t be measured or seen Fluid losses from the skin and lungs SENSIBLE LOSS Fluid losses from urination, defecation, wounds, and other means that can be measured  THIRD-SPACING occurs when too much fluid moves from the intravascularLoading… space (blood vessels) into the interstitial or "third" space-the nonfunctional area between cells  CAUSES Third-space shifts occur in ascites, burns, peritonitis, bowel obstruction, and massive bleeding into a joint or body cavity. MANIFESTATIONS URINE OUTPUT Early clue of third space fluid shift despite adequate fluid intake Fluids shifts out of the intravascular space Kidneys receive less blood compensation Decrease urine output MANIFESTATIONS Increase heart rate Decrease blood pressure Decrease central venous pressure Edema Increase body weight Intake and output imbalance  CELL MEMBRANE PUMPS Hydrostatic pressure Osmotic pressure Pressure exerted by the Exerted by the protein fluid on the walls of plasma to stop the flow of water by blood vessels osmosis  REGULATION OF BODY FLUID COMPARTMENTS Osmosis Fluid shifts through the membrane from the region of low solute concentration to the region of high solute concentration Movement of water across the semipermeable membrane Osmolality Tonicity -number of dissolved -ability of the particles contained in a unit of fluid solutes to cause an -concentration of fluid osmotic driving force  REGULATION OF BODY FLUID COMPARTMENTS Diffusion Movement of ions from area of higher concentration to one of lower concentration  REGULATION OF BODY FLUID Sodium-potassiumCOMPARTMENTS pump Actively moves sodium from the cell into the ecf and maintain high potassium concentration into the ICF  ACTIVE TRANSPORT Energy that is expended for the movement to occur against a concentration gradient ATP ROUTES OF GAINS AND LOSSES Kidneys Urine output- 1-2L/day in adult 1mL/kg/hr Skin Sensible perspiration depending on the temp Insensible perspiration Approximately 600mL/day ROUTES OF GAINS AND LOSSES Lungs Eliminates water through insensible loss 400mL/day GI tract 100-200mL/day intake volume output volume Oral liquids 1300ml urine 1500 Water in 1000ml food stool 200 Water 300 Insensible 900 produced by loss metabolism TOTAL 2600 TOTAL 2600 LABORATORY TEST FOR EVALUATING FLUID STATUS  OSMOLALITY Measures the solute concentration per kilogram in blood and urine Serum osmolality Reflects the concentration of sodium Urine osmolality Determined by urea, creatinine and uric acid Most reliable indicator of urine concentration Milliosmoles/kg of water (mOsm/kg)  Osmolality is the number of milliosmoles of solute (the standard unit of osmotic pressure) per kilogram of solvent; it is expressed as milliosmoles per kilogram (mOsm/kg) Osmolarity is the number of milliosmoles (the standard unit of osmoticpressure) per liter of solution; it is expressed as milliosmoles per liter (mOsm/L). URINE SPECIFIC GRAVITY BUN Measures the ability Made up of urea of the kidney to 10-20mg/dL (3.5-7mmol/L) excrete or conserve Factors in the elevation of BUN Decrease renal function, GI bleeding, water dehydration, increase protein intake, fever, sepsis 1.010-1.025 Factors decreasing BUN Less reliable ESRD Low protein diet starvation CREATININE HEMATOCRIT End product of muscle metabolism Volume percentage of RBC in BETTER INDICATOR OF WB RENAL FUNCTION 44-52-males 0.7-1.5mg/dL (60-130 mmol/L 39-47 in females URINE SODIUM 50-220mEq/24h Random specimen- 40mEq/L FLUID VOLUME DISTURBANCES Loading…  FLUID VOLUME DEFICIT Hypovolemia Loss of ECF volume exceeds the intake of fluid When water and electrolyte are lost in the same proportion  TYPES OF FLUID VOLUME DEFICITS 1.Isotonic dehydration Water and dissolved electrolytes are lost in equal proportions. Known as hypovolemia, isotonic dehydration is the most common type of dehydration. Isotonic dehydration results in decreased circulating blood volume and inadequate tissue perfusion.  TYPES OF FLUID VOLUME DEFICITS 2.Hypertonic dehydration Water loss exceeds electrolyte loss. The clinical problems that occur result from alterations in the concentrations of specific plasma electrolytes. Fluid moves from the intracellular compartment into the plasma and interstitial fluid spaces, causing cellular dehydration and shrinkage.  TYPES OF FLUID VOLUME DEFICITS 3.Hypotonic dehydration Electrolyte loss exceeds water loss. The clinical problems that occur result from fluid shifts between compartments, causing a decrease in plasma volume. Fluid moves from the plasma and interstitial fluid spaces into the cells, causing a plasma volume deficit and causing the cells to swell.  CAUSES 1.Isotonic dehydration Inadequate intake of fluids and solutes Fluid shifts between compartments Excessive losses of isotonic body fluids 2.Hypertonic dehydration conditions that increase fluid loss, such as excessive perspiration, hyperventilation, ketoacidosis, prolonged fevers, diarrhea, early-stage kidney disease, and diabetes insipidus  CAUSES 3.Hypotonic dehydration Chronic illness Excessive fluid replacement (hypotonic) Kidney disease Chronic malnutrition  MANIFESTATIONS Acute weight loss Flattened neck veins Decrease skin turgor Increase temperature Oliguria Decrease central venous Concentrated urine pressure Postural hypotension Cool, clammy skin Weak rapid CR Thirst, nausea, anorexia, muscle weakness  MEDICAL MANAGEMENT Replacement of fluid loss Monitor I and O Assess weight, vs, level of consciousness, breath sounds, skin color If oliguric- “fluid challenge test”  NURSING MANAGEMENT 1.Monitor cardiovascular, respiratory, neuromuscular, renal, integumentary, and gastrointestinal status. 2.Prevent further fluid losses and increase fluid compartment volumes to normal ranges. 3.Provide oral rehydration therapy if possible and IV fluid replacement if the dehydration is severe monitor intake and output.  NURSING MANAGEMENT 4.In general, isotonic dehydration is treated with isotonic fluid solutions, hypertonic dehydration with hypotonic fluid solutions, and hypotonic dehydration with hypertonic fluid solutions. 5.Administer medications, such as antidiarrheal, antimicrobial, antiemetic, and antipyretic medications, as prescribed to correct the cause and treat any symptoms. 6.Monitor electrolyte values and prepare to administer medication to treat an imbalance, if present  FLUID VOLUME EXCESS Isotonic expansion of the ECF caused by the abnormal retention of water and sodium Due to increase in the total body sodium content  TYPES OF FLUID VOLUME Isotonic overhydration EXCESS a.Known as hypervolemia, isotonic over hydration results from excessive fluid in the extracellular fluid compartment. b.Only the extracellular fluid compartment is expanded, and fluid does not shift between the extracellular and intracellular compartments. c. Isotonic overhydration causes circulatory overload and interstitial edema; when severe or when it occurs in a client with poor cardiac function, heart failure and pulmonary edema can result.  TYPES OF FLUID VOLUME EXCESS Hypertonic overhydration a.The occurrence of hypertonic overhydration is rare and is caused by an excessive sodium intake. b.Fluid is drawn from the intracellular fluid compartment; the extracellular fluid volume expands, and the intracellular fluid volume contracts.  TYPES OF FLUID VOLUME EXCESS Hypotonic overhydration a.Hypotonic overhydration is known as water intoxication. b.The excessive fluid moves into the intracellular space, and all body fluid compartments expand. c.Electrolyte imbalances occur as a result of dilution.  CAUSES Isotonic overhydration Hypotonic overhydration a.Inadequately controlled IV therapy a.Early kidney disease b.Kidney disease b.Heart failure c.Long-term corticosteroid therapy c.Syndrome of inappropriate Hypertonic overhydration antidiuretic hormone a.Excessive sodium ingestion secretion b.Rapid infusion of hypertonic saline d.Inadequately controlled IV c.Excessive sodium bicarbonate therapy therapy  MEDICAL MANAGEMENT Discontinue excessive Nutritional therapy administration of sodium- Dietary restriction containing fluid of sodium administer diuretics restrict fluid intake  Pharmacologic therapy Diuretics Hemodialysis Thiazide Renal function is so Blocks sodium reabsorption in the severely impaired distal tubule Removes nitrogenous Loop diuretics Blocks reabsorption of water and wastes and control sodium in the ascending loop of henle potassium and acid base Spironolactone balance Works in the last distal tubule of the nephrons  NURSING MANAGEMENT 1.Assess vital sign 6.Monitor weight daily 2.Position client in semi-fowler’s position 7.Assess for edema 3.Administer diuretics as prescribed 8.Provide a low sodium diet 4.Restrict fluid as prescribed 9.Monitor laboratory values 5.Monitor I & O *A client with acute kidney injury or chronic kidney disease is at high risk for fluid volume excess.  ELECTROLYTES Are chemicals that form electrically charged particles (ions) to make sure the body runs at optimal levels Active chemicals  CHARGES OF ELECTROLYTES Cations Anions Positive charges Negative charges Sodium, potassium, calcium, Chloride, bicarbonate, magnesium, hydrogen phosphate, sulfate, proteinate Unit of measurement meq/L  IN A SOLUTION CATIONS=ANIONS electrolytes measurement electrolytes measurement CATIONS IN Anions in ECF ECF Chloride 103 SODIUM 142 Bicarbonate 26 Potassium 5 Phosphate 2 calcium 5 sulfate 1 Organic acids 5 magnesium 2 proteinate 17 total 154 total 154 electrolytes measurement electrolytes measurement CATIONS IN Anions in ICF ICF Potassium 150 Phosphate and 150 Sulfate magnesium 40 Proteinate 40 Sodium 10 10 Bicarbonate total 200 total 200 ELECTROLYTE IMBALANCES  SODIUM Establish the electro chemical state necessary for muscle contraction and transmission of nerve impulses NORMAL VALUE: 135-145 mEq/L is a major cation of extracellular fluid it maintains osmotic pressure and acid-base balance and transmits nerve impulses absorbed from all intestine and excreted in urine in amounts dependent on dietary intake minimum daily requirement of Na is 15 mEq/L  SODIUM CONTAINING FOOD: COMMON TABLE SALT CORN FLAKES BACON PROCESSED OAT CEREALS CORNED BEEF CRACKERS FRANKFURTERS GREEN OLIVES LUNCH MEAT PICKLES BOUILLON CUBES PRETZELS CHEESE PROCESSED SALAD DRESSING BREAD STUFFING MIXES SOY SAUCE KETCHUP  SODIUM DEFICIT (HYPONATREMIA) a sodium deficit in which there is too little sodium in the serum, less than 135 mEq/L Sodium imbalances usually are associated with fluid volume imbalances.  CAUSES 1.Increased sodium excretion a.Excessive diaphoresis b.Diuretics c.Vomiting d.Diarrhea e.Wound drainage, especially gastrointestinal f.Kidney disease g.Decreased secretion of aldosterone  CAUSES 2.Inadequate sodium intake a.Fasting; nothing by mouth status b.Low-salt diet 3.Dilution of serum sodium a.Excessive ingestion of hypotonic fluids or irrigation with hypotonic fluids b.Kidney disease c.Freshwater drowning d.Syndrome of inappropriate antidiuretic hormone secretion e.Hyperglycemia f.Heart failure  NURSING INTERVENTIONS 1.Monitor cardiovascular, respiratory, neuromuscular, cerebral, renal, and gastrointestinal status. 2.If hyponatremia is accompanied by a fluid volume deficit (hypovolemia), IV sodium chloride infusions are administered to restore sodium content and fluid volume. 3.If hyponatremia is accompanied by fluid volume excess (hypervolemia), osmotic diuretics may be prescribed to promote the excretion of water rather than sodium.  NURSING INTERVENTIONS 4.If caused by inappropriate or excessive secretion of antidiuretic hormone, medications that antagonize antidiuretic hormone may be administered 5.Instruct the client to increase oral sodium intake as prescribed and inform the client about the foods to include in the diet 6.If the client is taking lithium,monitor the lithium level, because hyponatremia can cause diminished lithium excretion, resulting in toxicity *Hyponatremia precipitates lithium toxicity in a client taking lithium.  DILUTIONAL HYPONATREMIA Serum sodium level is diluted by an increase in the ratio of water to sodium Causes SIADH Hyperglycemia Increase water intake Use of tap water enemas Irrigation of ngt with water instead of NSS  SIADH Syndrome of inappropriate antidiuretic hormone Excessive ADH activity will result to water retention and dilutional hyponatremia Causes Oat-cell lung tumors Head injuries Endocrine and pulmonary disorders Physiologic or psychological stress  MANIFESTATIONS headache If below 115 mEq/L nausea and vomiting disorientation Signs of ICP frequent urination Lethargy Poor skin turgor Confussion Dry mucosa Decrease saliva production Focal weakness, Orthostatic hypotension hemiparesis Abdominal cramping Seizures Altered mental status MEDICAL NURSING MANAGEMENT MANAGEMENT Assessment Identification of patient at risk for hyponatremia Sodium replacement Monitor I and O Water restriction Weigh pt daily Monitor changes in LOC  SODIUM EXCESS (HYPERNATREMIA) a condition in which the serum sodium concentration is greater than 145 mEq/L  CAUSES 1.Decreased sodium excretion a.Corticosteroids b. Cushing’s syndrome c.Kidney disease d.Hyperaldosteronism 2.Increased sodium intake: Excessive oral sodium ingestion or excessive administration of sodium-containing IV fluids 3.Decreased water intake: Fasting; nothing by mouth status 4.Increased water loss: Increased rate of metabolism, fever, hyperventilation, infection, excessive diaphoresis, watery diarrhea, diabetes insipidus  CLINICAL MANIFESTATIONS Thirst Primarily neurologic symptoms and cellular Primary dehydration characteristics Moderate Restlessness and weakness Dehydration Severe Dry, swollen tongue and Disorientation sticky mucous Delusions membranes Hallucinations Brain damage  Nursing management Medical management 1.Monitor cardiovascular, respiratory, Gradual lowering of neuromuscular, cerebral, renal, and the serum sodium level integumentary status. Diuretics 2.If the cause is fluid loss, prepare to administer IV infusions. 3.If the cause is inadequate renal excretion of sodium, prepare to administer diuretics that promote sodium loss. 4.Restrict sodium and fluid intake as prescribed  CALCIUM NORMAL VALUE: 4.5-5.5 mEq/L or 9-10 mg/dL A cation that is absorbed into the bloodstream from dietary sources and functions in bone formation, nerve impulse transmission and contraction of myocardial and skeletal muscles aids in blood clotting by converting prothrombin to thrombin  CALCIUM FOOD SOURCES: CHEESE COLLARD GREENS KALE MILK AND SOY MILK RHUBARB SARDINES TOFU YOGURT  HYPOCALCEMIA A severe calcium deficit below 4.5 mEq/L or 9 mg/dL  CAUSES 1.Inhibition of calcium absorption 2.Increased calcium excretion from the gastrointestinal tract a.Kidney disease, polyuric phase a.Inadequate oral intake of calcium b.Diarrhea b.Lactose intolerance c.Steatorrhea c.Malabsorption syndromes such as d.Wound drainage, especially celiac sprue or Crohn’s disease gastrointestinal d.Inadequate intake of vitamin D e.End-stage kidney disease  CAUSES 3.Conditions that decrease the ionized fraction of calcium a. Hyperproteinemia b.Alkalosis c. Medications such as calcium chelators or binders d.Acute pancreatitis e. Hyperphosphatemia f.Immobility (prolonged) g. Removal or destruction of the parathyroid glands  INTERVENTIONS 1.Monitor cardiovascular, respiratory, neuromuscular, and gastrointestinal status; place the client on a cardiac monitor. 2.Administer calcium supplements orally or calcium intravenously. 3.When administering calcium intravenously, warm the injection solution to body temperature before administration and administer slowly; monitor for electrocardiographic changes, observe for infiltration, and monitor for hypercalcemia. 4.Administer medications that increase calcium absorption a.Aluminum hydroxide reduces phosphorus levels, causing the counter effect of increasing calcium levels. b.Vitamin D aids in the absorption of calcium from the intestinal tract.  INTERVENTIONS 5.Provide a quiet environment to reduce environmental stimuli. 6.Initiate seizure precautions. 7. Move the client carefully, and monitor for signs of a pathological fracture. 8.Keep 10% calcium gluconate available for treatment of acute calcium deficit 9.Instruct the client to consume foods high in calcium Figure 2 Tests for hypocalcemia. A, Chvostek’s sign is contraction of facialmuscles 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 (C) above the systolic pressure for a few minutes.  HYPERCALCEMIA a serum level that exceeds 11 mg/dL or 5.5 mEq/L  Causes 1.Increased calcium absorption a.Excessive oral intake of calcium b.Excessive oral intake of vitamin D 2.Decreased calcium excretion a.Kidney disease b.Use of thiazide diuretics  Causes 3.Increased bone resorption of calcium a.Hyperparathyroidism b.Hyperthyroidism c.Malignancy (bone destruction from metastatic tumors) d.Immobility e.Use of glucocorticoids 4.Hemoconcentration a. Dehydration b.Use of lithium c.Adrenal insufficiency  Interventions 1.Monitor cardiovascular, respiratory, neuromuscular, renal, and gastrointestinal status; place the client on a cardiac monitor. Loading… 2.Discontinue IV infusions of solutions containing calcium and oral medications containing calcium or vitamin D. 3.Thiazide diuretics may be discontinued and replaced with diuretics that enhance the excretion of calcium.  Interventions 4.Administer medications as prescribed that inhibit calcium resorption from the bone, such as phosphorus, calcitonin, bisphosphonates, and prostaglandin synthesis inhibitors (acetylsalicylic acid, nonsteroidal antiinflammator medications). 5.Prepare the client with severe hypercalcemia for dialysis if medications fail to reduce the serum calcium level. 6.Move the client carefully and monitor for signs of a pathological fracture. 7. Monitor for flank or abdominal pain,and strain the urine to check for the presence of urinary stones. 8.Instruct the client to avoid foods high in calcium  *A client with a calcium imbalance is at risk for a pathological fracture. Move the client carefully and slowly; assist the client with ambulation Assessment Findings HYPOCALCEMIA HYPERCALCEMIA Cardiovascular▪ Decreased heart rate▪ Hypotension▪ Increased heart rate in the early phase; bradycardia Diminished peripheral pulses ▪ that can lead to cardiac arrest in late phasesIncreased blood pressure Respiratory▪ Not directly affected; however, respiratory failure or arrest can result from decreasedrespiratory movement Bounding, full peripheral pulses because of muscle tetany or seizures Ineffective respiratorymovement as a result of profound Neuromuscular▪ Irritable skeletal muscles: Twitches, cramps, skeletal muscle weakness tetany, seizures ▪ Painful muscle spasms in the calf or foot during periods of inactivity ▪ Paresthesias followed by Profound muscle weakness Diminished or absent deep numbness that may affect the lips, nose, and ears in addition to tendon reflexes the limbs▪ Positive Trousseau’s and Chvostek’s signs▪ Hyperactive deep tendon reflexes▪ Anxiety, irritability Disorientation, lethargy, coma Renal▪ Urinary output varies depending on the cause Urinary output varies depending on the cause Gastrointestinal▪ Increased gastric motility; hyperactive bowel Decreased motility and hypoactive bowel sounds sounds▪ Cramping, diarrhea Anorexia, nausea, abdominal distention, constipation Laboratory Findings▪ Serum calcium level less than 9.0 mg/ dL Serum calcium level that exceeds 10.5 mg/ Dl (2.75 (2.25 mmol/L) ▪ mmol/L) ▪ Electrocardiographic changes: Prolonged ST interval,  MAGNESIUM NORMAL VALUE: 1.5- 2.3 mEq/L or 1.8-2.6 mg/dL Used as an index to determine metabolic activity and renal function needed in the blood-clotting mechanism, regulates neuromuscular activity, acts as a cofactor that modifies the activity of many enzymes and has an effect on the metabolism of calcium  COMMON FOOD SOURCES: AVOCADO PEANUT BUTTER, ALMONDS CANNED WHITE TUNA PEAS CAULIFLOWER PORK, BEEF, CHICKEN, SOYBEANS GREEN LEAFY VEGETABLES, SUCH AS POTATOES SPINACH AND BROCCOLI RAISINS MILK YOGURT OATMEAL, WHEAT BRAN  HYPOMAGNESEMIA A decreased serum magnesium level of less than 1.5 mEq/L or 1.8 mg/dL  CAUSES 1. Insufficient magnesium intake a.Malnutrition and starvation b.Vomiting or diarrhea c. Malabsorption syndrome d. Celiac disease e. Crohn’s disease  CAUSES 2. Increased magnesium excretion a.Medications such as diuretics b. Chronic alcoholism 3. Intracellular movement of magnesium a. Hyperglycemia b. Insulin administration c. Sepsis  INTERVENTIONS: 1.Monitor VS 2.Monitor for dysrhythmias 3.Monitor for neuromuscular changes 4.Monitor I&O 5.Initiate seizure precaution 6.Administer oral or IV magnesium Oral preparations of magnesium may cause diarrhea and increase magnesium loss.  INTERVENTIONS: 7.Monitor calcium and potassium levels and administer calcium and potassium as prescribed if levels are low 8.Monitor serum magnesium levels every 12-24 hours when client is receiving magnesium by IV 9.Monitor for reduced deep tendon reflexes 10.Instruct client to eat foods high in magnesium, calcium and potassium  HYPERMAGNESEMIA an increased magnesium serum level of 2.3 mEq/L or 2.5 mg/dL  CAUSES 1.Increased magnesium intake a.Magnesium-containing antacids and laxatives b. Excessive administration of magnesium intravenously 2.Decreased renal excretion of magnesium as a result of renal insufficiency  INTERVENTIONS 1.Monitor cardiovascular, respiratory, neuromuscular, and central nervous system status; place the client on a cardiac monitor. 2.Diuretics are prescribed to increase renal excretion of magnesium. 3.Intravenously administered calcium chloride or calcium gluconate may be prescribed to reverse the effects of magnesium on cardiac muscle.  INTERVENTIONS 4.Instruct the client to restrict dietary intake of magnesium-containing foods 5.Instruct the client to avoid the use of laxatives and antacids containing magnesium. *Calcium gluconate is the antidote for magnesium overdose. TABLE 2.1G Assessment Findings HYPOMAGNESEMIA HYPERMAGNESEMIA Cardiovascular▪ Tachycardia ▪ Bradycardia, dysrhythmias Hypertension Hypotension Respiratory▪ Shallow respirations Respiratory insufficiency when the skeletal muscles of respiration are involved Neuromuscular▪ Twitches, paresthesias▪ Positive Diminished or absent deeptendon Trousseau’s and Chvostek’s signs▪Hyperreflexia▪ reflexesSkeletal muscle weakness Tetany, seizures Drowsiness and lethargy that progresses to Central Nervous System▪ Irritability ▪ Confusion coma Laboratory Findings▪ Serum magnesium level less Serum magnesium level thatexceeds 2.1 than 1.3 mEq/L (0.65 mmol/L)▪ ▪ mEq/L(1.05 mmol/L)Electrocardiographic Electrocardiographic changes:Tall T waves, changes:Prolonged PR interval, widened depressed ST segments QRS complexes  PHOSPHOROUS NORMAL VALUE: 3.0-4.5 mg/dL or 1.8-2.6 mEq/L important in bone formation, energy storage and release, urinary acid-base buffering, and carbohydrate metabolism high concentrations of phosphorous are stored in bone and skeletal muscle is absorbed from food and excreted by the kidneys  COMMON FOOD SOURCES: DAIRY PRODUCTS FISH NUTS PORK, BEEF, CHICKEN, ORGAN MEATS PUMPKIN, SQUASH WHOLE-GRAIN BREADS AND CEREALS  HYPOPHOSPHATEMIA a serum phosphate below 3.0 mg/dL or below 1.8 mEq/L A decrease in the serum phosphorus level is accompanied by an increase in the serum calcium level.  Causes 1.Insufficient phosphorus intake: Malnutrition and starvation 2.Increased phosphorus excretion a.Hyperparathyroidism b.Malignancy c.Use of magnesium-based or aluminum hydroxide–based antacids 3.Intracellular shift a.Hyperglycemia b. Respiratory alkalosis  ASSESSMENT 1.Cardiovascular a.Decreased contractility and cardiac output b. Slowed peripheral pulses 2.Respiratory: Shallow respirations 3.Neuromuscular a.Weakness b.Decreased deep tendon reflexes c.Decreased bone density that can cause fractures and alterations in bone shape d.Rhabdomyolysis  ASSESSMENT 4.Central nervous system a.Irritability b.Confusion c.Seizures 5.Hematological a.Decreased platelet aggregation and increased bleeding b.Immunosuppression  INTERVENTIONS 1.Monitor cardiovascular, respiratory, neuromuscular, central nervous system, and hematological status 2.Discontinue medications that contribute to hypophosphatemia. 3.Administer phosphorus orally along with a vitamin D supplement. 4.Prepare to administer phosphorus intravenously when serum phosphorus levels fall below 1 mg/ dL and when the client experiences critical clinical manifestations.  INTERVENTIONS 5.Administer IV phosphorus slowly because of the risks associated with hyperphosphatemia. 6.Assess the renal system before administering phosphorus. 7.Move the client carefully, and monitor for signs of a pathological fracture. 8. Instruct the client to increase the intake of the phosphorus- containing foods while decreasing the intake of any calcium- containing foods  *A decrease in the serum phosphorus level is accompanied by an increase in the serum calcium level, and an increase in the serum phosphorus level is accompanied by a decrease in the serum calcium level. This is called a reciprocal relationship.  HYPERPHOSPHATEMIA a serum phosphate level greater than 4.5 mg/dL or 2.6 mEq/L Most body systems tolerate elevated serum phosphorus levels well. An increase in the serum phosphorus level is accompanied by a decrease in the serum calcium level. The problems that occur in hyperphosphatemia center on the hypocalcemia that results when serum phosphorus levels increase.  Causes 1.Decreased renal excretion resulting from renal insufficiency 2. Tumor lysis syndrome 3. Increased intake of phosphorus, including dietary intake or overuse of phosphate-containing laxatives or enemas 4. Hypoparathyroidism  ASSESSMENT Cardiovascular▪ Decreased heart rate▪ Hypotension▪ Diminished peripheral pulses ▪ Respiratory▪ Not directly affected; however, respiratory failure or arrest can result from decreasedrespiratory movement because of muscle tetany or seizures Neuromuscular▪ Irritable skeletal muscles: Twitches, cramps, tetany, seizures ▪ Painful muscle spasms in the calf or foot during periods of inactivity ▪ Paresthesias followed by numbness that may affect the lips, nose, and ears in addition to the limbs▪ Positive Trousseau’s and Chvostek’s signs▪ Hyperactive deep tendon reflexes▪ Anxiety, irritability Renal▪ Urinary output varies depending on the cause Gastrointestinal▪ Increased gastric motility; hyperactive bowel sounds▪ Cramping, diarrhea  INTERVENTIONS 1. Interventions entail the management of hypocalcemia. 2. Administer phosphate-binding medications that increase fecal excretion of phosphorus by binding phosphorus from food in the gastrointestinal tract. 3. Instruct the client to avoid phosphate-containing medications, including laxatives and enemas. 4. Instruct the client to decrease the intake of food that is high in phosphorus