studying fluid and electrolytes hope this helps everyone gl with nclex :redpinkhe :redpinkhe fluid and electrolytes 1. the two major fluid compartments in the body are intracellular and extra cellular a. sodium and chloride are the major electrolytes in intracellular fluid. b. calcium and bicarbonate are also extracellular electrolytes. c. potassium, phosphate, and magnesium are the most plentiful intracellular electrolytes. 2. organs and glands in electrolyte balance a. lungs and liver: regulate sodium and water balance and blood pressure. b. heart secretes anp (atrial natriuretic peptide) a cardiac hormone causing sodium excretion. 1. the actions of anp oppose those of the renin-angiotensin-aldosterone system. 2. anp decreases blood pressure and reduces intravascular blood volume. 3. atrial stretching increases the amount of anp released. c. sweat glands excrete sodium, potassium, chloride, and water through sweat. d. gi tract: absorbs and excretes fluid and electrolytes. e. parathyroid glands - secrete parathyroid hormone which draws calcium into the blood and helps move phosphorus to the kidneys for excretion. f. thyroid gland secretes calcitonin, which prevents calcium release from the bone 3. movement through capillaries a. fluids and solutes move through capillary walls to help maintain fluid balance. b. hydrostatic pressure (pressure of blood pushing against capillary walls) forces fluid and solutes through the walls. c. when the hydrostatic pressure inside a capillary is greater than the pressure in the surrounding interstitial space, fluids and solutes inside the capillary are forced into the interstitial space. d. when the pressure inside a capillary is less than the pressure outside it, fluids and solutes move back into the capillary. e. realabsorption prevents excessive amount of fluid from leaving the capillaries. f. within the capillaries, albumin acts like a water magnet to attract and hold water inside the vessel - known as the plasma colloid osmotic pressure. g. as long as hydrostatic pressure exceeds plasma colloid pressure, water and solutes can leave the capillaries and enter interstitial fluid. if not, water and solutes return to the capillaries. 4. kidneys a. in the kidneys, nephrons filter about 180 l of blood daily -> this amount is the glomerular filtration rate. b. nephrons produce 1-2 l of urine daily. c. the kidneys conserve water or excrete excess fluid to maintain balance. 5. adh (anti-diuretic hormone) - vasopressin. a. regulates fluid balance b. secreted from the posterior pituitary, produced by hypothalamus. c. adh restores blood volume by reducing diuresis and increasing water retention. d. the single most important effect of adh is to conserve body water by reducing the loss of water in urine. e. adh increases blood volume and blood pressure. f. how adh works: the hypothalamus senses low blood volume and increased serum osmolality and signals the pituitary gland -> the pituitary gland secretes adh into the bloodstream -> adh causes the kidneys to retain water -> water retention boosts blood volume and decreases serum osmolality. 6. spacing a. first spacing - normal distribution of fluid in the intracellular fluid. b. second spacing - an abnormal accumulation of interstitial fluid (edema). c. third spacing - occurs when fluid accumulates in a portion of the body from which it is not easily exchanged with the rest of the ecf - is any fluid not where it is supposed to be (ascites). 7. renin-angiotensin-aldosterone system a. helps maintain a balance of sodium and water, a healthy blood volume and pressure. b. when the fluid or sodium level falls, the juxtaglomerular cells secrete renin, which stimulates angiotensin ii production. c. angiotensin ii causes vasoconstriction and stimulates aldosterone production. d. aldosterone causes sodium and water retention leading to increased fluid volume and sodium levels. e. when b/p returns to normal, the body halts the release of renin, which stops this system. f. how aldosterone works: aldosterone ii stimulates the adrenal gland to release aldosterone -> aldosterone causes the kidneys to retain sodium and water -> sodium and water retention leads to increases in fluid volume and sodium levels. 8. major electrolytes a. sodium - 135-145 - remember: brain doesn't like it when na is messed up 1. is the major ecf cation. the na level in the blood is totally dependent on how much water there is in the body. 2. helps nerve cells and muscle cells interact. aids in impulse transmission. 3. helps maintain appropriate ecf osmolality. 4. maintains ecf volume and influences body water distribution. 5. affects the concentration, excretion and absorption of potassium and chloride. 6. the kidneys regulate na excretion through aldosterone action. 7. increased na level in the ecf results in decreased aldosterone production, which increases renal na excretion. 8. increased na level in the ecf also raises ecf osmolality, which stimulates adh release that ^'s renal water reabsorption. 9. decreased na level in the ecf results in increased aldosterone production, which decreases renal na excretion. 10. decreased na level in the ecf also lowers ecf osmolality, which inhibits adh release and increases renal water excretion. 11. hyponatremia - too much water, not enough na. a. sodium deficit b. excessive na loss or an excessive water gain in the ecf. c. etiology: prolonged diuretic therapy, excessive diuresis, insufficient na intake, gi fluid losses, cystic fibrosis, burns, siadh, hypotonic fluids. d. in a nutshell sodium loss or water gain increases or na intake decreases -> fluid moves by osmosis from the extracellular space (which has more water and less sodium) into the more concentrated intracellular space -> cells contain more fluid and blood vessels contain less. cerebral edema and hypovolemia can occur. e. s/s: headache, muscle cramps/twitching, hypotension, tachycardia, faintness, decreased urine output, decreased skin turgor, altered loc, dry mucous membranes, nausea and seizures. note: symptoms of hypernatremia are related to cellular swelling and are first manifested in the cns. f. laboratory 1. elevated hematocrit and plasma proteins. 2. urine specific gravity less than 1.010 3. increased urine specific gravity and urine sodium level in patient with siadh. g. treatment 1. restrict fluid intake as ordered, patient needs sodium, not water. 2. with severe hypernatremia, serum na concentration should not be raised by more than 12 meq/l during the first 24 hours. 3. monitor v/s, especially b/p and pulse rate, skin integrity, daily weights. 4. isotonic or hypertonic iv saline solutions cautiously to avoid inducing hypernatremia from excessive or too-rapid infusion, use infusion pump. 12. hypernatremia - too much na, not enough water. a. increased serum na levels usually indicate a water deficit in the ecf, which moves water out of the icf to equilibrate. b. cellular shrinkage results from increased na levels in the ecf increasing serum osmolality and water movement from the icf into the ecf. c. cellular shrinkage in the cns causes impaired cns and cognitive function. d. in a nutshell sodium intake or water loss becomes excessive -> serum osmolality increases -> fluid moves by osmosis from inside of the cells to outside of the cells to balance intracellular and extracellular fluid levels -> cells become dehydrated causing neurologic impairment, extracellular fluid volume in vessels increases causing hypervolemia. e. etiology: significantly deficient water intake, hypertonic fluids & tube feedings, excessive salt intake, diabetes insipidus, aldosteronism, severe diarrhea, heat stroke, high fever, hyperosmolar hyperglycemic nonketonic syndrome (hhnks) f. s/s: extreme thirst, dry mouth, swollen tongue, decreased loc, hallucinations, s/s from hypervolemia (from na gain) such as bounding pulses and hypertension. low grade fever. g. laboratory 1. urine specific gravity greater than 1.030 2. serum na level greater than 145 3. in diabetes insipidus patients, urine specific gravity is less than 1.005. h. treatment 1. restrict sodium intake. 2. dilute patient with iv fluids. replace fluids gradually over 48 hours to avoid shifting water into brain cells. if too much water is replaced too quickly, water moves into brain cells and they swell causing cerebral edema. usually d5w, hypotonic solutions. use salt-free solutions. 3. assess neurologic status. 4. monitor serum na levels, urine specific gravity, fluid i & o, and daily weights (same time every day, same clothes, same scale). monitor labs. b. potassium - 3.5 to 5.0 1. is the major cation in the icf. responsible for cell excitability, nerve impulse conduction, resting membrane potential, muscle contraction, myocardial membrane responsiveness, and intracellular osmolality. 2. is excreted by the kidneys. 3. potassium is found in saliva, perspiration, and stomach and intestinal secretions. 4. potassium directly affects cardiac muscle contraction and electrical conductivity. 5. potassium aids neuromuscular transmission of nerve impulses. 6. potassium plays a major role in acid-base balance; any alteration in k balance will result in acid-base imbalance. 7. potassium must be ingested daily because the body does not conserve it. 8. potassium is lost in the kidneys and bowel. any alteration in bowel influences potassium absorption. 9. potassium and na have a reciprocal relationship; the feedback mechanism regulating na excretion is opposite that regulating k excretion. 10. aldosterone secretion leads to renal na reabsorption and k excretion. 11. hyperkalemia a. results from impaired renal excretion or excessive k intake. b. hyperkalemia is the most dangerous electrolyte imbalance. even a slight increase in the potassium level can profoundly affect the neuromuscular and cardiovascular system. 1. excessive serum k levels act as a myocardial depressant causing decreased heart rate, decreased cardiac output, and possible cardiac arrest. 2. hyperkalemia causes skeletal muscle weakness, usually the initial symptom that causes patients to seek health care assistance. c. etiology: acute or chronic renal failure, increased k intake especially with decreased urine output. k supplements, salt substitutes, diuretics, burns, trauma, intravascular hemolysis, hyponatremia, d. in a nutshell potassium intake increases or potassium excretion decreases -> k+ shifts out of cells into extracellular fluid -> extracellular k+ level rises -> patient develops neuromuscular and cardiac signs and symptoms. e. s/s: begins with muscle twitching, apathy, diarrhea, bradycardia, confusion, paresthesia/numbness in extremities, abdominal cramps, muscle weakness/paralysis, oliguria. decreased heart rate, irregular pulse. f. laboratory 1. serum k level greater than 5.5 meq/l 2. decreased arterial ph indicating acidosis. 3. widened qrs complex, depressed st segment - can lead to asystole. g. treatment 1. restrict potassium intake 2. dialysis if kidneys aren't working 3. patients with significant hyperkalemia should be monitored by ecg to detect dysrhythmias. 4. be prepared to give calcium gluconate by slow iv infusion in acute cases while potassium is being eliminated and forced into cells. it counteracts the myocardial depressant effects of hyperkalemia & decreases arrhythmias. 5. monitor cardiac status, v/s, k levels, 6. administer regular insulin and hypertonic dextrose by iv to move potassium into the cells. during therapy monitor for hypoglycemia. 7. administer sodium bicarb (kayexalate) to a patient with acidosis to shift k into the cells. exchanges na for k in the gi tract. 8. hyperkalemic patients taking digitalis glycosides cannot receive calcium; administering calcium gluconate with digitalis may exacerbate the effects of digitalis leading to digitalis toxicity. 9. monitor for hyponatremia in patients receiving sodium bicarb. 10. teach patients, especially those with renal failure, about foods high in potassium to avoid them and to avoid salt substitutes. foods high in potassium include spinach, bananas, mustard greens, brussel sprouts, eggplant, tomatoes, apricots, bell pepper, strawberries, tuna, oranges, lima beans, potatoes (white or sweet), cabbage, halibut, avocado. 12. hypokalemia a. usually results from excessive excretion or inadequate intake of k+. b. potassium balances na in the ecf to maintain electroneutrality of body fluids. sodium and potassium have an inverse relationship. c. the most common causes are from abnormal losses via either the kidneys or the gi tract. abnormal losses occur when the patient is diuresing, particularly in the patient with elevated aldosterone level. d. occurs because the patient cannot effectively conserve potassium. e. in a nutshell potassium intake decreases or potassium loss increases-> k+ shifts from extracellular fluid to intracellular fluid -> intracellular k+ levels rise -> cells cant function properly -> muscular, gi, and cardiac dysfunctions occur. f. etiology: prolonged diuretic therapy, severe diaphoresis, stress, hepatic disease, renal defect, cushing syndrome, alcoholism, tumors of the adrenal cortex. ng suction, vomiting, not eating. g. s/s: muscle cramps & weakness, arrhythmias, n/v, decreased bowel motility (ileus), pvc's, hypotension, drowsiness and lethargy. h. laboratory 1. ecg changes, depressed st segment, flattened t waves, characteristic u waves. 2. urine specific gravity less than 1.010 3. elevated ph and bicarb levels. i. treatment 1. restore potassium balance. infuse slowly 2. place patient on high potassium diet. 3. to prevent gastric irritation from oral potassium supplements, administer them with at least 4 ounces of fluid or food 4. if patient on digitalis, monitor for digitalis toxicity. 5. monitor i & o, v/s, potassium levels, heart rate, pulse. 6. never give potassium by iv push or bolus, is fatal. 7. monitor iv site for complications. k is highly irritating. 8. potassium rich foods: banana's, oranges, apples, broccoli, cantaloupe, apples. spinach, mustard greens, brussel sprouts, eggplant, tomatoes, apricots, bell pepper, strawberries, tuna, oranges, lima beans, potatoes (white or sweet), cabbage, halibut, avocado. c. calcium - 9.0-10.5 mg/dl *** acts like a sedative *** if you want to get calcium questions right think muscles first 1. stabilizes cell membranes and reduces permeability, transmits nerve impulses, contracts muscles, coagulates blood, and forms bones and teeth. 2. calcium is the major cation involved in the structure and function of bones and teeth. 3. calcium and phosphorus have an inverse relationship -> increased calcium level results in decreased serum phosphorus level, and decreased calcium level results in increased serum phosphorus level. 4. calcium helps maintain cell membrane structure, function, and membrane permeability. 5. calcium affects activation, excitation, and contraction of cardiac and skeletal muscle. 6. calcium is absorbed in the small intestine in the presence of vitamin d. 7. vitamin d promotes ca absorption; phosphorus inhibits ca absorption. 8. parathyroid hormone (pth) promotes ca transfer from bone to plasma and aids intestinal and renal ca absorption. 9. almost 50% of serum ca is bound to serum albumin; thus, albumin levels must be considered with ca levels. 1. a decrease in albumin will lower ca level. 2. an increase in albumin will raise the ca level. 10. hypocalcemia - not enough sedative a. decreased ca level stimulates pth release from the parathyroid glands; this releases calcium phosphate from bone and indirectly activates mechanisms to increase ca reabsorption and phosphorus excretion from the renal tubules and the gi tract. 1. in a nutshell ca absorption decreases -> parathyroid gland releases pth -> pth draws calcium from bone & promotes renal reabsorption & intestinal absorption of ca -> lack of ca outstrips pth's ability to compensate -> ca is no longer available to maintain cell structure and function -> patient develops neuromuscular and cardiac symptoms & decreased loc. b. results from hypoparathyroidism, thyroidectomy, decreased ca intake, severe diarrhea, laxative abuse, high phosphorus levels, pancreatitis, reduced gastric acidity, massive blood transfusions, alkalosis. drugs that can decreased ca: lasix, phosphates, phenobarb, cisplatin, gentamicin, calcitonin. c. s/s: anxiety, confusion, arrhythmias, decreased cardiac output, hyperactive dtr's, paresthesia of toes, fingers or face (especially around the mouth), spasms of laryngeal and abdominal muscles, tetany, tremors, twitching, muscle cramps, swallowing problems, laryngospasm, loc changes. **trousseau's sign and chvosteks's sign. d. laboratory 1. ecg changes: lengthened qt interval and prolonged st segments 2. calcium level less than 8.2 mg/dl e. treatment 1. iv calcium gluconate or calcium chloride - widens qrs. do not administer too quickly, give via infusion pump because infiltration can cause tissue necrosis and syncope, hypotension, and arrhythmias. place patient on cardiac monitor to detect any changes in heart rate and rhythm, especially if patient is receiving digoxin. 2. assess iv site for infiltration 3. give magnesium with calcium because hypocalcaemia doesn't respond to calcium therapy alone. 4. diet: high calcium and high protein. 5. administer a phosphate binder - amphogel, antacid to lower an elevated phosphorus level. cannot give to renal patients because they cant get rid of the aluminum and will get toxic. 6. if patient begins to complain of flushing and sweating when giving magnesium, stop infusion. for asystole give atropine or epinephrine. 7. keep tracheotomy tray and resuscitation bag nearby in case patient develops laryngospasm. 8. assess for chvostek's sign and trousseau's sign. 9. institute seizure precautions. 11. hypercalcemia - too much sedative a. elevated ca level stimulates the thyroid gland to release calcitonin, which inhibits ca release from bone and reduces pth production (pth makes ca go up) and release, thereby decreasing mobilization, intestinal absorption, and ca reabsorption by the kidneys. b. in hypercalcemia, the rate of ca entry into extracellular fluid exceeds the rate of ca by the kidneys. c. in a nutshell ca resorption from bone increases -> ca enters extracellular fluid at an increased ed rate ->ca movement into extracellular fluid exceeds the rate of ca by the kidneys-> excess ca enters cells -> excess intracellular ca decreases cell membrane excitability -> reduced membrane excitability affects skeletal and cardiac muscles & the nervous system -> patient may display fatigue and decreased loc. d. results from increased ca resorption from bone, hyperparathyroidism, increased ca absorption or decreased ca excretion, hyperthyroidism, fractures, prolonged immobilization, hypophosphatemia. antacids that contain calcium. e. s/s: weak and brittle bones, kidney stones, abdominal pain & constipation, behavioral changes with confusion, bone pain, decreased loc, extreme thirst, polyuria, hypoactive dtr's, muscle weakness, n/v, hypertension, f. test/laboratory 1. ecg changes - shortened qt intervals and shortened st segments 2. elevated serum digoxin levels in a patient receiving digoxin. 3. x-rays showing pathologic fractures. g. treatment 1. have patient move around/ambulate 2. limit dietary intake of ca and discontinue drugs that contain calcium. add phosphorus to diet - any protein food has phosphorus in it. 3. hydrate patient with ns to promote diuresis and ca excretion. 4. administer loop diuretic (lasix) to help promote ca excretion. 5. don't give thiazide diuretic to a patient hypercalcemia because it can inhibit calcium excretion. 6. possible dialysis if ca levels too high. 7. corticosteroids to block bone resorption and decrease gi absorption of calcium. 8. give phospho soda & fleets enema - both have phosphorus. 9. assess for arrhythmias, renal calculi. 10. assess for digoxin toxicity if patient is receiving digoxin. 11. calcitonin decreases serum ca, it drives ca back into the bone. d. magnesium - 1.2 - 2.1 meq/l ***think muscles first when mg is involved.*** 1. responsible for enzyme reactions, neuromuscular contractions, normal functioning of nervous and cardiovascular systems, protein synthesis, and sodium and potassium ion transportation. 2. acts like a sedative. 3. activates intracellular enzymes and acts in carbohydrate and protein metabolism. 4. affects peripheral vasodilation resulting in changes in blood pressure and cardiac output. 5. magnesium facilitates na and k+ across cell membranes. 6. influences intracellular ca level through its effect on pth secretion. 7. is secreted by kidneys and it can be lost other ways (gi tract). 8. hypermagnesemia a. results from renal dysfunction, advanced age, renal failure, addison's disease, adrenocortical insufficiency, dka, excessive mg intake. b. magnesium makes you vasodilate -> is a vasodilator -> will increase b/p c. in a nutshell magnesium excretion decreases or mg intake increases -> high mg level suppresses acetylcholine release at myoneural junctions ->reduced acetylcholine blocks neuromuscular transmission and decreases cell excitability -> the neuromuscular and cns systems become depressed -> loc decreases and respiratory distress occurs -> arrhythmias and other cardiac complications may develop. d. drugs that can cause hypomagnesaemia: antacids, laxatives that contain magnesium and magnesium supplements. e. s/s: bradycardia, decreased loc progressing to lethargy to coma, decreased muscle and nerve activity, flushed skin and feelings of warmth, hyperactive dtr's, hypotension, generalized weakness, n/v, decreased respirations & respiratory arrest. f. laboratory/test 1. ecg changes - prolonged pr interval, widened qrs complex, tall t-waves 2. serum magnesium levels greater than 2.6 meq/l g. treatment 1. if patient has normal renal function, increase iv fluids to rid body of excessive magnesium 2. calcium gluconate at bedside. calcium gluconate in the presence of magnesium will inactivate each other. administer very slowly (max rate is 1.5-2 ml/min). a. calcium gluconate toxicity = give magnesium sulfate 1. b = b/p decreased 2. u = urine output decreased 3. r = respiratory rate decreased 4. p = patellar reflexes absent 3. be prepared for dialysis and mechanical ventilation if respirations 4. assess dtr's and muscle strength, flushing and diaphoresis. 5. closely monitor respiratory status. 6. monitor for fluid overload 7. avoid use of drugs that contain magnesium and restrict dietary intake of magnesium. 9. hypomagnesemia a. hypomagnesemia results from excessive mg loss from increased renal excretion or gi fluid losses, insufficient dietary mg intake, or movement of mg from ecf to icf. b. magnesium is the second most abundant intracellular cation, is essential for neuromuscular integration; hypomagnesmia increases muscle cell irritability and contractility. c. causes decreased b/p and may result in ventricular arrhythmias. d. caused by alcoholism, inadequate gi absorption (ulcerative colitis, crohn's disease, bowel resection, pancreatic insufficiency, pancreatitis, diarrhea), hyper/hypo parathyroidism, dka, renal disease/insufficiency. excessive intake of vitamin d or ca, burns, gentamicin, pih. e. in a nutshell magnesium intake or absorption decreases or magnesium loss increases -> mg moves out of cells to compensate for low extracellular level -> cells become starved for mg -> skeletal muscle weakness and nerves and muscles become hyperirritable. f. laboratory/test 1. ecg changes - prolonged pr intervals, widened qrs complex, prolonged qt intervals, depressed st segments, prominent u waves. 2. other electrolyte abnormalities - hypocalcemia, hypokalemia. g. s/s: tachycardia and other arrhythmias, tremors, tetany, hyperactive dtr's, positive chvostek's and trousseau's sign, positive babinski reflex, h. drugs that can cause hypomagnesemia: insulin, cisplatin, laxatives, loop diuretics, amphotericin b, cyclosporine, thiazide diuretics. i. treatment 1. monitor patients at risk for hypo-mg, particularly those with hypokalemia, and those receiving tpn without mg replacement. monitor ca levels. 2. give magnesium: before administering mg, assess renal function -> if urine output 10 ml in 4 hours, monitor mg level closely -> kidneys excrete magnesium. administer mg slowly -> can cause cardiac/respiratory arrest 3. assess dtr's if absent, hold and notify md 4. assess for laryngeal stridor which may indicate onset of airway obstruction. 5. monitor for dysphasia - swallowing may be impaired. 6. monitor for chvostek's and trousseau's sign, babinski reflex, 7. institute seizure precautions. 8. monitor digoxin levels if patient on digoxin for toxicity. iv fluids 1. isotonic a. go in the vascular space and stays there b. use isotonic solutions in irrigations, infusions, etc, unless a specific aim is to shift fluid to intracellular or extracellular spaces. c. used to treat dehydration. d. types of isotonic fluids 1. normal saline 2. lactated ringers 3. 5% dextrose in water (d5w) 2. hypotonic a. go into the vascular space, hang out for a bit and rehydrate, but do not stay in the vascular space then they move into the cell and the cell burns the remainder up in cellular metabolism. b. they are hydrating solutions. indicated for cellular dehydration. c. they do not cause the pressure to go up because they do not stay in the vascular space. if they stayed in the vascular space they would be an isotonic solution d. hypotonic solutions have less salt or more water than an isotonic solution e. cause the fluid to move from ecf to the icf. f. types 1. 0.5% normal saline (hns or 0.45% ns) 2. 2.5% dextrose in 0.45% saline 3. nacl 3. hypertonic a, indicated for intravascular dehydration with interstitial or cellular over hydration b used with extreme caution c. is a volume expander and solution that draws fluids into the vascular space. draws water out of the cell. d. types 1. 5% dextrose in lactated ringers 2. 5% dextrose in 0.45% saline 3. 5% dextrose in 0.9% saline 4. tpn 4. tip: 1. isotonic solutions stay where i put it. hypotonic solutions "go out of the vessel" hypertonic solutions "enter the vessel" 2. iv tubing and dressing should be changed by hospital policy (usually every 72 hours. 3. flushing a saline lock requires approximately 1-½ times the amount of fluid the tubing will hold. use sterile technique to prevent complications 4. flow rate calculations a. ml/hr. total ml fluid to be given/total hrs = ml/hr b. gtts/min. total ml fluid to be given/total min to be administered x gtt/ml = gtt/min