OK I know this sounds stupid but I have a friend that gets really freaked out before big tests like finals, HESI, NCLEX, and usually we get together and a few days before I start throwing out random facts at her. On 2 different tests she said the only way she got several questions was from the random facts that I threw at her that she never would have thought of!
SOOOOO..... I thought that if yall wanted to do this we could get a thread going and try to throw out 5 random facts or "things to remember". NCLEX is coming and the more I try to review content the more I realize that I have forgotten so......here are my 5 random facts for ya:
OH and BTW these came from rationales in Kaplan or Saunders no made up stuff:
1️⃣ A kid with Hepatitis A can return to school 1 week within the onset of jaundice.
2️⃣ After a patient has dialysis they may have a slight fever...this is normal due to the fact that the dialysis solution is warmed by the machine.
3️⃣ Hyperkalemia presents on an EKG as tall peaked T-waves
4️⃣ The antidote for Mag Sulfate toxicity is ---Calcium Gluconate
5️⃣ Impetigo is a CONTAGEOUS skin disorder and the person needs to wash ALL linens and dishes seperate from the family. They also need to wash their hands frequently and avoid contact.
Oh, ohh, one more...
? Vasopressin is also known as antidiuretic hormone
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.
*** 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.
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.
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
OK I am puzzled and I need some help. Is HHNK, HHNC, HHNS all the same thing? Have been studying diabetes for NCLEX
HHNK = hyperosmolar hyperglycemic nonketosis = the diagnosis
HHNC = hyperosmolar hyperglycemic nonketosis coma = late stage of the condition
HHNS = hyperosmolar hyperglycemic nonketotic syndrome (see definition below)
If the same is ok but if not, how are they treated differently for purposes of NCLEX? CAN ANYONE PLEASE HELP ME?
Syndrome= a complex of signs and symptoms resulting from from a common cause or appearing in combination to present a clinical picture of a disease or inherited abnormality.
HHNS= a serious condition seen most frequently in older people and can happen with either type I or II diabetes, but it is seen more often on diabetes type II patients. HHNS is usually brought by something else such as an illness or and infection.
Warning Signs:
blood sugar level 600 mg/dl or greater
dry, parched mouth
extreme thirst (although it may gradually disappear)
warm, dry skin that does not sweat
high fever (over 101º F)
sleepiness or confusion--decreased LOL
loss of vision
hallucinations
weakness on one side of the body
Ketoacidosis= a serious condition that leads to diabetic coma due to dangerous high levels of ketones in the blood. Ketones are the by product of fat metabolism, and they appear in the urine when the body does not have enough insulin, in starvation, high protein, low carbohydrate and high fat diets. Ketoacidosis happens to people with diabetes type I, only. Diabetes type II patients get HHNS.
Warning Signs:
Early symptoms:
thirst or a very dry mouth
frequent urination
high blood glucose levels (240 mg/dl and up)
high levels of ketones in the urine (normally there should be no ketonespresent in the urine
Late symptoms:
constantly feeling tired
dry or flushed skin
nausea/vomiting or abdominal pain
difficulty breathing: short, deep breaths (Kussmaul's respiration)
fruity odor on breath
decreased LOL, confusion, hard time paying attention when spoken to
When blood glucose is 240 mg/dl or higher check for ketones in the urine, that has to be done every 4 hrs when blood sugar is 240 mg/dl or greater or any of the typical symptoms of ketoacidosis are observed in a
diabetes type I patient. I hope this information helps. feliz3
I want to add a comment about Regular insulin which besides been clear is the only one of the insulin types that can be given intravenously. If you see on an NCLEX scenario which says "insulin was given IV..." you immediately assume safely that the type of insulin given was Regular for that is the only of the insulin types that can be given by the IV route. feliz3
taking nclex tomorrow - please pray. why does it seem that no matter how much you study you never seem to know enough? lol
growth and development for pediatrics
pediatrics
1. motor skills progress in a proximal to distal manner.
2. neonate (birth to 28 days):
a. vital signs:
1. pulse: 110 - 160 bpm count apical for one minute
2. respiratory rate: 32 - 60 bpm. neonate is an obligate nose breather.
3. blood pressure: 82/46.
4. temperature regulation is altered because of poorly developed sweating and shivering mechanisms.
a. limit exposure time during baths.
b. when the neonate is wet or cold cover his head.
5. mortality rate is higher in the neonatal period than in any other growth stage.
b. head and chest circumference are relatively equal. head circumference may be up to ¾ greater than the chest circumference.
c. head length is one-fourth total body length.
d. brain growth depends on myelinization.
e. all behavior is under reflex control. extremities are flexed.
1. moro reflex- elicited by striking a flat surface the infant is lying on. the reflex of abducting extremities and fanning fingers when a sound is heard should be gone by 3-4 months. strongest at 2 months
2. rooting - when the cheek of the newborn is stroked, the newborn will turn his head in the direction of the stroke. usually disappears 3-4 months
3. tonic neck - while the newborn lies supine, his head is turned causing the extremities on the same side to straighten and those on the opposite side to flex (fencing posture). disappears at 3-4 months.
4. babinski - when the sole of the foot on the side of the newborn small toe is stroked upward, the toes will fan upward and out
5. plantar grasp - infant's toes will curl downward when sole of foot is touched.
6. startle - a loud noise such as a hand clap will elicit the newborn to abduct his arms and flex his elbows. best elicited after infant is at least 24 hours old and disappears within 4 months.
7. palmar/plantar grasp - place a finger in the palm of the newborn's hand and then place a finger at the base of the toes, the newborn's fingers and toes curl downward.
f. hearing and touch are well developed; a hearing screening is recommended.
g. the neonate is stimulated by being held or rocked; listening to music and watching a black-white mobile.
h. while laying prone, the neonate can lift his head.
3. infancy: age 1 month to 1 year.
a. period of rapid growth in which the head, especially the brain, grows faster than other tissues.
b. according to erickson, the infant is in the critical stage of trust vs. mistrust. it is important for the child to develop a trusting relationship with a consistent primary caregiver. interference may cause failure the thrive.
c. birth weight doubles in 6 months.
d. birth weight triples in one year.
e. posterior fontanel closes by 2-3 months.
f. anterior fontanel remains open until 18 months.
g. height increases by 50% in 1 year.
h. head circumference > than chest circumference until 1 year.
i. tooth eruption starts at 4 months -> 1 tooth per month.
j. ages 1 to 4 months
1. instinctual smile appears at age 3 months. the social smile is the infants first social response. the social smile initiates social relationships, indicates memory traces, and signals the beginning of thought processes.
2. the infant develops binocular vision; the eyes can follow an object 180 degrees and any intermittent strabismus should be resolved by age 4 months.
3. the infant reaches out voluntarily but uncoordinatedly.
4. at age 4 months the infant laughs in response to environment.
5. recognizes parents voices.
6. explores his feet.
7. appropriate toys: music box, mobile, mirror.
k. ages 5-6 months
1. birth weight doubles.
2. can sleep through the night with 1-2 naps a day.
3. lower central incisors appear first. results in 'ed drooling and irritability.
4. rolls over from stomach to back.
5. infant cries when parents leave - a normal sign of attachment. exhibits stranger anxiety.
6. can transfer toys from one hand to another
7. exhibits comforting habits - sucks thumb, rubs his ears, holds a blanket or stuffed toy.
a. all these symbolize parents and security.
b. thumb sucking in infancy doesn't result in malocclusion of permanent teeth.
2. creeps on his hands and knees with his belly off of the floor.
3. infant stands and stays up by grasping for support.
4. develops a pincer grasp; places everything in his mouth - 'ed risk of aspiration.
5. self-feeds crackers; the infant who's physically and emotionally ready can begin to be weaned to a cup.
6. likes to look at self in mirror.
7. develops object permanence and searches for objects outside his perceptual field.
8. understands the word "no"; discipline can begin. cries when reprimanded.
9. can verbalize consonants but speaks no intelligible words. 10. appropriate toys: peek-a-boo, cloth toys.
m. ages 10 - 12 months
1. birth weight triples and birth length increases about 50%.
2. imitative behaviors.
3. infant cruises (takes steps while holding on) at age 10 months, walks with support at 11 months, and stands alone and takes his first steps at 12 months.
4. infant claps his hands, waves bye-bye and enjoys rhythm games.
5. enjoys books and toys to build with and knock over.
6. cooperates when dressed.
7. can say mama/dada and two syllable words.
8. shows jealousy.
9. infant explores everything by feeling, pushing, turning, pulling, biting, smelling, and testing for sound.
10. appropriate toys: push toys, large ball, large blocks.
n. nutrition
1. introduce foods in this sequence
a. breast milk or iron-fortified formula: according to aap (american academy of pediatrics) they recommend breast feeding exclusively for the first 4-6 months of life and then in combination with infant foods until age 1.
1. give breast fed infants iron supplements after age 4 months because iron received before birth is depleted.
2. breast milk is a rich source of linoleum acid (essential fatty acid) and cholesterol which are needed for brain development.
3. contains immune factors that protect infants from infection.
b. don't give solid foods for the first 6 months
1. before age 6 months, the gi tract tolerates solid food poorly.
2. because of strong extrusion reflex, the infant pushes food out of his mouth.
3. the risk of food allergy development may increase.
c. provide rice cereal as the first solid food followed by any other cereal except wheat.
d. give yellow or green vegetables next.
e. provide no citrus fruits followed by citrus fruits after age 6 months.
f. give infants teething biscuits during teething period.
g. provide food with sufficient protein such as meat, after age 6 months.
h. after 12 months, switch from formula to regular whole milk.
1. don't give skim milk because fatty acids are needed for myelinization.
2. whole milk should be continued until age 2 as recommended by the aap.
i. rules for feeding
1. don't prop up baby bottle - 's risk of aspiration & ear infections.
2. don't put food or cereal in a baby bottle.
3. introduce one new food at a time; wait 4-7 days before introducing new food to determine infant's tolerance to it and the potential for allergy.
o. safety guidelines
1. place infants supine for sleep to decrease the risk of sudden infant death syndrome.
2. keep crib rails up at all times, keep away from windows and curtain cords. crib slats should not be more than 2" apart with mattress firmly against its rails to prevent infant falling in-between mattress and slats.
3. use car seats properly - keep infant placed facing back of back seat.
4. never leave infant unattended on dressing table or any other high place.
5. don't warm formula or breast milk in microwave. defrosting in microwave may destroy its immune factors. formula/food should be lukewarm.
6. insert safety plugs in wall outlets
7. use gates along stairways.
8. keep soft objects and loose bedding out of the crib. pillows, quilts, sheepskins and comforters should be kept out of infant's sleeping environment.
9. avoid overheating; infant should be lightly clothed for sleep.
10. always support infants head.
11. check temperature of bath water - should be 90-100 degrees.
p. toddler (ages 1 to 3)
1. vital signs: pulse 100 bpm
respiratory rate: 26 bpm
blood pressure: 99/64
2. period of slow growth with a weight gain of 4-6 lbs per year. normally weighs four times birth weight.
3. anterior fontanel closes between ages 12 and 18 months.
4. the toddler is egocentric.
5. follows parents wherever they go.
a. start playing peek-a-boo to develop trust.
b. progress to playing hide and seek to reinforce the idea that his parents will return.
6. separation anxiety arises.
a. the toddler sees bedtime as desertion.
b. develops a fear of the dark. nightmares begin around 2-3.
c. separation anxiety demonstrates closeness between the toddler & his parents.
d. the parent who is leaving should say so and should promise to return.
1. parent should leave a personal item with the toddler.
2. prepare the parents for the toddlers reaction, and explain that this process promotes trust.
e. according to erickson, this is the critical stage of autonomy (self control & will power) vs shame. the child develops a sense of independence and should be allowed to explore the environment with the encouragement of the primary caregiver. temper tantrums, negativism, and disciplinary problems are the hallmarks of this age group as the child learns to control his environment and express his will. the child should be taught to tolerate frustration through socialization and proper toilet training.
1. according to freud, toddlers are egocentric and possessive and struggle with holding on and letting go behaviors (anal stage).
2. toddlers usually begin to imitate sex role behavior.
3. piaget: sensorimotor stage the child enters the pre-operational stage in which he begins using a trial and error method of thinking and reasoning.
f. the toddler may engage in solitary play and have little interaction with others, this progresses to parallel play (toddler plays along-side but not with other children.
g. to promote development of autonomy, allow the toddler to perform tasks independently and provide choices.
h. toddler understands object permanence.
i. discipline during this stage should be a demonstration of love, not anger. the toddler needs limits set on unacceptable demands, such limits offer security. he should be praised liberally, but only when deserved.
j. things to expect:
1. sphincter control begins at age 2.
2. all deciduous teeth erupt by 21 months - 2 years.
3. pot-bellied appearance.
k. 18 months
1. is in the "my" stage. 2. vocabulary of 25 words.
3. walks independently 4. can use a spoon.
5. climbs.
appropriate toys: push/pull toys, blocks.
l. 24 months
1. negativistic 2. temper tantrums
3. transitional object 4. 2-4 word sentences, 400 words
10. manage temper tantrums: ignore behavior, monitor for safety.
11. toddler uses "no" excessively and shows assertiveness. is curious how parents will react to use of "no".
12. overcriticizing and restricting the toddler may dampen his enthusiasm and increase shame and doubt.
13. total sleep required is 12-14 hours. sleep problems are common.
14. toilet training
a. consider emotional readiness
b. the toddler acts to please others, trusts enough to give up his body products, and begins autonomous behavior
c. parents must be committed to establishing a toileting pattern and must communicate well with the toddler.
d. offer praise for success - never punishment for any failure.
e. don't refer to bowel movements as being "dirty" or "yucky". excrement is the toddler's first creation.
f. introduce underpants as a badge of success and maturity.
g. most toddlers achieve day dryness by age 18 months to 3 years and night dryness by ages 2-5. never punish for "accidents". if toddler is not trained by age 5, seek further evaluation.
h. toddler may fear being "sucked" into the toilet.
i. teach proper wiping technique (front to back) and hand washing.
j. toilet training - when kid can communicate need to go (non verbal or verbal), holds on to please mom and doesn't let go to please self, sphincter control 18 months - 24 months (myelination of the cord is complete now), motor skill. ability to stay dry for 2 hours, can sit still on toilet for 5 - 10 minutes without fussing, curiosity about older people's habits. no right or wrong time !
15. when the toddler starts climbing over the crib rails, switch to a bed.
16. use locks on cabinets, keep handles away from edges of tables or stoves.
17. avoid bean bag toys.
18. appropriate toys: nested toys, toys with parts that open and close. toys designed for pounding such as play hammers and drums. toy telephones, dolls. provide the child with opportunities for positive imitative play. they enjoy simple songs with repetitive rhymes as well as moving in time to music. a musical activity should be scheduled into each day.
19. nutrition:
a. toddler feeds himself, provide finger foods in small portions
b. because of increased risk of aspiration avoid foods such as hot dogs, grapes, nuts and candy (or cut into small pieces).
c. nutritional needs decrease because of slow growth period.
d. child may become a picky eater. nutritional content of food is important.
e. the toddler shouldn't drink more than 24 ounces of milk a day in order to have room for other nutritious food.
milestones
by age 3:
able to jump in place able to kick a ball
able to ride a tricycle able to state name, age, and gender
able to copy a cross and circle most speech is understandable by others
by age 4:
able to sing simple songs able to draw a person with 3 or more body parts
able to distinguish between reality and fantasy
able to state first and last name
able to build tower with at least 10 blocks
able to hop on one foot at least 3 times
able to throw ball over handed all speech is understandable
by age 5: (enters kindergarten)
able to dress self without assistance
able to state entire name (first, middle, and last)
able to state home address and home phone number
able to follow 2-3 step directions
able to count to 10 on fingers
able to copy a triangle or square
able to draw a person with head, body, and all extremities
able to recognize most letters of the abc's and able to print a few
plays "make believe"
by age 6:
able to walk heel/tow forward and backwards
able to hop on either foot
able to catch baseball size ball with 2 hands
able to feed self correctly using knife, fork, and spoon
able to cut out simple shapes with scissors
able to distinguish between right and left hand
able to play games involving matching skills
able to repeat simples nursery rhymes
able to choose peers for play
is protective of younger siblings
nclex questions
1. when does birth length double - by 4 years
2. when does child sit unsupported - by 8 months
3. when does a child achieve 50% of adult height - 2 years
4. when does a child throw a ball overhand - 2 years
5. when does a child speak 2-3 word sentences - 2 years
6. when does a child use scissors - 4 years
7. when can a child tie his/her shoes - 5 years
8. girl's growth spurt during adolescence begins earlier than boys. may begin as early as 10 years old.
9. temper tantrums are common in the toddler; they are considered normal or average behavior.
10. adolescence is a time when the child forms his/her identity and that rebellion against family values is common for this age group.
good luck everyone with nclex :flowersfo:flowersfo:flwrhrts::flwrhrts::flwrhrts::levcmmt:
just want to thank you very much for all of your postings. i'm as well taking mine tomm,neclex rn:stone. much luck to you:coollook: i was brushing up on some of the child devp. and according saunders by 6 they tie their shoes. so is it between the ages 5 and 6 that they can tie their shoes is it really at 5yrs old they can. well, everyone please pray for us that we pass the neclex rn. also i wan to thank the rest of the peeps. that are also using inputing their info. on this thread.
mine is also tomorrow and thanks for the post mamaellis2many .i found your post very easy to keep in mind .if anything new and mandatory for tomorrow ,please post for us...thankyou and wish you all the best!
nclex is over with and lord help me. just a general question: if there is a prolapsed cord wouldnt the first intervention be to place mom knee chest rather than notify md? isnt a tb patient confined to his room and not able to walk around the unit?
talk about feeling like failing, i am now asking myself where the frig did they come up with all those meds that i have never heard of in my life. i have never been made to feel so stupid and know so little.
it cut off at 121 questions and the first time i took it, it stopped at 141 - bad or good?
i feel sorry for my poor family and friends to have to put up with this angst for a few days. i just walked away thinking i studied so hard to know so little. god and i became very close during that exam because i found myself praying after a few of the questions. couldn't pick answer c on any of my questions, lol because they were obviously so wrong, lol
while there, there were several cardiologist takinig some test that was required and i could hear one of them cussing lol. i told the ladies there at least i know i was in good hands if i went into cardiac arrest.
all i can say for those who took the exam is good luck. now let's sit and hope for the best and know that deep down we know we have studied hard and if by chance any of us fail, to try and try again. we worked this hard to come this far and lets all be danged if we will give up on our dreams of being a nurse.
:flowersfo:flowersfo:flwrhrts::flwrhrts::flwrhrts::levcmmt:
mamaellis2many
37 Posts
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