Chapter 16 Lewis : Fluid & Electrolytes

What happens with fluid (ECF/ICF) when pt is in FVD?

fluid shift from (intracellular) cell to (extracellular) interstitial and vascular (blood vessels) why???? to compensate for LOW fluid volume so not enough fluid in vascular system and other ECF areas so the cell gives up its fluid to interstitial space and into vascular system in order to fix the deficit (recording 18 min on 1/15)

What is hypernatremia as far as ECF/ICF?

fluid shift from cells to ECF via osmosis

What mechanisms control fluid & electrolyte movement?

hydrostatic pressure - push osmotic oncotic pressure - colloid pull (albumin) diffusion - solute moves - "stuff" - high [] to low [] facilitated diffusion - osmosis - water moves low to high active transport NA& K pump

with HYPONATREMIA the bowels will be?

hyperactive

Immobile patients can develop

hypercalcemia you need exercise to move ca+ into bones <<<?? check recording to make sure

RELATIONSHIP of metabolic alkalosis/acidosis w/ calcium (hyper/hypo_

hypercalcemia = high ca+ = low pH = acidic (metabolic) hypocalcemia = low ca+ = high pH = alkalosis (metabolic)

tetany occurs w/ what electrolyte imbalance?

hypocalcemia

What patient should be doing weight-bearing exercises?

hypocalemic because decreases ca+ bone loss

in hyponutremic patients we should try what first? and what is the amount we do it in?

fluid restriction 500 mL less than the previous 24 urine output example: person has output of 1000mL on 1/1 so on 1/2 they are restricted to only 500 mL of fluid in

Hypercalcemia can cause?

1. cardiac & smooth muscle activity to be decreased

average adult the kidneys will produce approx how much urine per day

1.5 L or 1500 mL

K+ losing diuretic

furosimide = Lasix (we lose it)

Medical management of hypermagnesmia?

1. avoid giving to PT w/ renal failure SEVERE EMERGENCY: IV calcium glucanate & ventialtory support 3. Loop Diuretics (ex: Lasix--furosimide) - loop means it acts at loop at henley in nephron - helps eliminate Mg level 4. hemodialysis - emergency means theyre getting hemodialysis

Hypermagnesemia causes?

1. blocks release of acetylcholine (causes contraction of muscles, activates contraction of muscles) from nerve cell junction --> results in ---> decreased cell activity if we have low levels of Mg then we aren't going to have muscle contractions

What does Na+ do in the body?

1. H2O balance - Na+ is magnet for H2O, it follows water 2. Nerve Transmission - conducts nerve impulses 3. Muscle Contraction - IMPORTANT = muscle = heart = problems

Hypomagnesemia: symptoms, signs, manifestations

1. anorexia, nausea 2. dysrhythmias/EKG changes 3. vasospasm 4. tetany/ tremors 5. depression/confusion/Psychosis 6. low level serum low Mg = LOW Ca+ typically < 2:06 REC

Nursing Management for Hypomagnesemia

1. assess EKG 2. monitor labs: Mg K Ca 3. assess neuro status 4. teach alcoholism & diet 5. dysphasia common in magnesium depleted pt ------assess ability to swallow w/ water before administering food or medications

What are s/s | manifestations of hypovolemia

- dark concentrated urine (oliguria) - weak, rapid pulse (HR) - low BP (hypotension) - poor/decreased turgor (tenting present) - cool skin (shunting to vital organs) - ^^ decreased cap refill - weak/dizzy --progressing to--> restlessness, drowsy, confusion (increased Na+)

Hyperkalemia and the ICF / ECF balance?

- elevated serum K+ decreases the concentration difference of K+ between ICF & ECF this increase - makes the cell MORE excitable - means heart is MORE excitable

Hypocalcemia can be caused by?

- poor intake Ca+ - Cushing's disease - poor absorption of Ca+ in gut [ pt w/ small intestine issues b/c small intestine absorbs electrolytes ] - vit D deficiency [ vit D = sunlight / some people don't have enough vit D = issues w/ Ca+ ] - malabsorption of fat - renal disease [ not retaining Ca+ ] - metabolic alkalosis - meds that cause Ca+ loss - loss of parathyroid gland

Manifestations of hypernatremia?

- restlessness, weakness, agitation, stupor, lethargy, coma (r/t Cerebral dehydration) - anorexia, nausea, & vomiting - dry flushed skin, dry mucous membranes - elevated body temp - seizures - elavated BP (hypervolemic) decreased BP (hypovolemic - weight gain/edema if increased sodium is due to excess sodium intake and not inadequate water intake - oliguria -- dark concentrated urine - increased urine specific gravity & osmolality

What nursing management should be done for a patient with FVE?

- semi-fowlers for orthopena - restrict fluids, restrict Na+ (for the two <<< we need to educate pt, pt family & post signs), diauretics (thiazide, Furosamide) - Assess I&O - teach diet, watch for OTC meds, watch for hidden Na+ sources - watch for decreasing edema - ASSESS I&O - cardiac + respiratory dysfunction --- monitor cap refill, SOB, pulse Ox - check edema: worse/better ****************BEST INDICATOR OF EDEMA IMPROVE OR DETERIORATING = DAILY WEIGHTS 2.2 lb = 1 kg = 1 L of fluid - skin care b/c edema = skin prone to break down, so position/turning = vital - if fluid will not come off w/ above tx then dialysis for renal failure pt - may need O2 admin PRN

What are clinical manifestations of Hypocalcemia?

- tetany (aka hyperrelfexiy) - cn calso cause stridor, dysphagia, paresthesia - specificially - trousseaus sign (bp cuff) - chvosteks sign (tap cheek) [parathyroid gland - dyspnea - increased peistalsis/diarrhea - prolonged Q-T interval ---cardiac issues - hypotension - dysrhythmias & seizures - prolonged bleeding times - numbness, tingling of lips, fingers & toes

What IV fluids are hypotonic?

1. 1/2 normal saline 0.45% 2. D51/2NS or D5W or D5 (same thing) *******D5 = VERY IMPORTANT TO NOTE***** D5 contains dextrose, dextrose is sugar, it is isotonic, but when dextrose is broken down it becomes hypOtonic

Hyperkalemia: nursing management

1. assess neuromuscular status [ due to hyper-excitable cells ] 2. monitor cardiac rhythm & EKG (watch for tenting of T wave) 3. monitor lab: K+ level & renal profile [looking at BUN & Creatinine to make sure renal function is okay] 4. monitor I&O (watch for oliguria/renal failure) 5. daily weights 6. invert IV bottles SEVERAL TIMES when K+ is mixed w/ fluid NEVER ADD K+ TO HANGING FLUIDS BOLUS MAY OCCUR 7. Low K+ diet 8. IF YOU DONT SEE PEE DONT GIVE K

Manifestations of hypophosphatemia?

1. CNS depression 2. Confusion 3. Muscle weakness & pain 4. Dysrhythmias 5. Cardiomyopathy (heart is getting larger to compensate) low phosphate = high Ca+ high Ca+= calmed down system

What are lab values we expect with FVE?

1. DECREASED serum osmolality 2. DECREASED H&H (b/c more fluid means HH is more dilute, or less concentrated) 3. DECREASED urine specific gravity = < 1.003 4. Serum Na+ could be increased, decreased or normal depending on amount of Na+ retention &/or H2O retention 5. pulmonary congestion - noted via Xray 6. ABGs 7. watch for drop in O2 8. change in acid-base balance 9. change in K+ level

Hyperkalemia = clinical symptoms

1. EKG changes ***************best indicator of intracellular K+ is a tall T-wave***************** 2. Tachycardia then Bradycardia ((why tachycardia = b/c cells are excited )) 3. hypotension 4. muscle spasticity ( highly excitable cells ) leading to weakness then paralysis 5. Nausea & EXPLOSIVE diarrhea (( GI is moving TOO fast b/c of excitability plus their body wants to remove excess K+) 6. weakened or arrested heart

What are some causes of hypokalemia?

1. GI K+ loss [ N+V patients ] 2. dietary changes [patients not ingesting enough] 3. medications = Lasix is a K+ LOSING diuretic) 4. movement of K+ like for example: K+ lost via kideny in aging pt inability to concentrate urine 5. various disorders i.e. - hyperaldosteronism [too much aldosterone which causes kidney to reabsorb more Na+ which means kidneys will lose K+ due to increasing aldosterone ] - anorexia 6. below normal serum potassium level which can occur with ALKALOSIS due to shift of serum potassium into cells

What is the nursing management for FVD?

1. I & O = for SEVERE FVD = MONITOR I & O EVERY HOUR using a special foley bag that has hourly I&O capabilities 2. VS = frequently 3. URINE OUTPUT = extremely important to show that their kidneys are functioning 4. monitor for symptoms of dehydration -- skin turgor, mucous membranes, mental status, skin & tongue (tongue will be dry, creased) 5. measures to minimize anymore fluid loss -- if from vomiting & diarrhea then we need MEDS to stop this 6. rest 7. oral care - from nausea & vomiting 8. administer oral fluids/IV fluids

Hypophosphatemia is caused by ?

1. Malnourishment/malabsorption [[chronic alcoholics from not eating, anorexic patients, kakectic < cancer patients ]] [[malabsorption in small intestine]] 2. ETOH withdrawal 3. Use of phosphate-binding antacids 4. Inadequate replacement during parenteral nutrition

What are manifestations of Hyponatremia?

1. N+V, abdominal cramps 2. hyperactive bowel sounds 3. headache, lethargy, confusion 4. weakness 5. dry skin & mucous membranes 6. poor skin turgor 7. tremor/convulsions 8. seizures, coma, if bad 9. deteriorating mentation

What IV fluids are isotonic?

1. Normal Saline (NS) 0.9% NaCl (sodium chloride) 2. Lactated Ringers (LR) --- plasma expander

What IV fluids are hypertonic?

1. TPN 2. D10 (10% dextrose) 3. 3% NS

What causes Hyperphosphatemia

1. acute kidney injury or chronic kidney disease [[cant get rid of P]] 2. chemotheraphy 3. excessive ingestion of phosphate in diet or Vitamin D [[phosphates come from food, you can over ingest them, very bad food has a LOT of phosphates]]

Hypokalemia nursing management

1. admin K+ replacement ((((((((((( NO IV PUSH, OR IM K+ MAKE SURE KCl is WELL DISTRIBUTED IN IV BAG ALWAYS GIVEN IN 1 L OF FLUID, 1000ML OF FLUID, YOU NEVER ADD K+ TO FLUID, THE PHARMACIST DOES THIS &&& IS ALWAYS GIVEN ON A PUMP ALWAYS ))))))))))))))[[[K+ IS TOXIC AND CAUSTIC TO VEIN WALLS, IF PT COMPLAINS OF PAIN YOU MAY NEED TO BACK OFF ON RATE OF INFUSION, ALWAYS ASSESS SITE FOR INFILTRATION, PROBLEMS]]]] 2. for PO replacement (quite common to give PO) give w/ full glass of water 3. monitor bowel status -hypoactive bowel sounds 4. monitor neuro status 5. monitor for digitalis toxicity [[digitalis helps heart pump better, people taking digoxin could become anoxic fast, one of the first systems of dig toxicity could lower, have bradycardia, you could draw a dig level to check, you could also see N+V & photosensitivity ]] 1:37min recording 6. monitor labs (K+, digitalis levels) 7. monitor urine output IF YOU DONT SEE PEE YOU DONT GIVE K B/C thats how they get rid of K+, it could become hyperkalemic VERY fast, dangerous

Hypocalcemia nursing management

1. administer Ca+ replacement 2. monitor cardiac rhythms 3. assess for trousseau's & chvostek's signs 4. monitor for increased bleeding 5. safety precautions - fall risk - pathologic fractures weak bones due to low Ca+ 6. montain high Ca+ diet 7. weight-bearing exercises to decrease bone calcium loss

Hypercalcemia nursing management

1. administer meds PRN 2. assess EKG changes 3. assess bowl sounds Q 8 hours 4. assess neuro status (mental changes typically reversible) 5. ****************push fluids unless contraindicated 3-4 L / daily***************************** 6. strain urine *renal calculi* 7. monitor labs: ca+

Hyponatremia nursing management?

1. administration of electrolyte & fluid replacement 2. monitor v/s 3. monitor neuro status 4. daily weights 5. monitor labs 6. maintain fluid restriction 7. observe for circulatory overload --- increased SOB, HR, RR < monitor for these things

Hypomagnesemia : Contributing factors:

1. alcoholism 2. malabsorption 3. malnutrition [[all 1-3 = PO issue of not taking in enough Mg]] 4. excess antacid intake (elderly) [[ taking TOO much, interfering w/ body ability to take in Mg]] 5. alkalosis 6. mads

Hypercalcemia manifests as?

1. anorexia, N+V & constipation 2. cardiac standstill/arrest ****** 3. dysrhythmias/heart block ***** [cardiac system = not as effective very sedated for low Ca+ level] 4. abdominal distension/ ileus [GI system slows] 5. confusion/lethargy/coma 6. kidney stones, renal failure [too much Ca+ accumulates & deposits making kidney stones which if they damage the nephrons = failure] 7. weakness & fatigue

Calcium does what for the body?

1. body's most abundant ion 2. works w/ P to make bones & teeth strong 3. determines strength & thickness of cell membranes 4. quiets nerve cells l/t smoother conduction of nerve impulses [ Ca+ = calming, settling effect on nerve impulses ] 5. important for manufacturing of clotting factors 6. assists in myocardial contractility 7. must have Vit D for absorption & use of Ca+ in body high P level = LOW Ca+ high Ca+ level = LOW P level need Vit D for Ca+ to work

What can bring on hypercalcemia?

1. bone cancer - Ca to ECF bone is being broken down, Ca+ is leached out and reaches ECF 2. hyperthyroidism - stimulates metabolism of bone which can cause Ca+ level to rise 3. hypophosphatemia - low phosphate = high Ca+ 4. metabolic acidosis - acidosis = renal problems typically - if metabolic acidosis = bad at excreting Ca+ 5. immobilization/medications - as you walk, Ca+ is being picked up by bone, if you aren't walking Ca+ is just hanging out and Ca+ is not being picked up by bone

What is medical management for hyperkalemia?

1. cardiac monitoring ((number 1 watch for lethal ventricular arrhythmia)) & IV calcium gluconate ((typically given in ICU IF PATIENT HAS LETHAL VENTRICULAR ARRHYTHMIA it is an antagonist to the cardiac conduction system, it levels things off and is always given on a pump)) (antagonizes cardiac conduction problems r/t K+) ((Ca+ is calming effect)) 2. increase fluids (increase urine output) [to remove K+ from system since its excreted in urine] 3. sodium bicarb IV (temporary shifts K+ into cells) [why? hyperkalemic patients are acidotic so we want to neutralize the acid which will help w/ K+] 4. K+ wasting diuretics - Lasix, Bumex, Thiazides, furosomide NEVER SPRINOLACTONE 5. insulin & hypertonic dextrose IV (causes K+ uptake into cell again this is temporary) [sometimes on insulin IV & YOU ONLY GIVE REGULAR INSULIN WHICH IS CLEAR TO HYPERKALEMIC PATIENTS---insulin = causes potaissum back into cell and gets it out of ECF, if you do this you need to give them sugar so D5 will be given to prevent hypoglycemic ] 6. KAYEXALATE BINDS W/ K+ IN BOWEL TO INDUCE K+ LOSS [ you have a lot of BM in these patients and a lot of diarrhea, can be given rectal or PO ] 7. Low K+ and HIGH carbohydrate diet [high potassium is healthy food, low in potassium is bad food, bread & pasta, processed food | cooked fruit & veg = water has potassium so throw away if trying to have low K+] 8. dialysis for severe renal failure

What lab data would you expect to see in someone w/ hypovolemia or fluid volume deficit?

1. elevated BUN in relation to serum Creatinine (BUN & Creatinine = tell us kidney function) 2. Increased H+H (Hematocrit is inversely proportional to fluids so, decreased fluid = increased H+H because H+H becomes more concentrated in the presence of less fluid)

What are some reasons people get hypernaturemia (types/causes < from slides thats what it says)

1. excessive Na+ intake 2. Inadequate water intake 3. excessive water loss 4. diseases

Hyponatremia can happen with?

1. excessive sodium loss 2. inadequate sodium intake 3. excessive water gain 4. diseases 5. adrenal insufficiency 6. water intoxication 7. SIADH or losses by vomiting, diarrhea, sweating, diuretics 8. N+V >> people just push water but not electrolytes, which = excess water = problem 9. diseases

What is sodium a good judge of in the body?

1. fluid levels FVE & FVD b/c its so important in water balance, sodium is a magnet for water, it draws water w/ it 2. nerve transmission conducts nerve transmission in nervous system - what is most important muscle in body? heart, so if Na+ is too low or too high you can have problems with your heart

What are clinical manifestations of hypermagnesemia?

1. flushing 2. lowered BP 3. N+V 4. Hypoactive reflexes 5. droswiness 6. muscle weakness 7. depressed respirations 8. ECG changes, dysrhythmias ** decreased cell activity = calming down --GI = hypoactive, constapation, decreased RR, decreased BM

What causes FVE

1. heart failure (CHF) 2. Liver Failure (hepatic issues---cirrhosis of liver) 3. renal failure in general: people who have problems regulating fluid volume balance

hyperphosphatemia can be managed how?

1. id & tx underlying cause 2. restrict foods& fluids containing phosphorus 3. phosphate-binding agents ((neutraphos)) 4. adequate hydration & corection of ypocalcemic conditions 5. hemodialysis, IV insulin & glucose (((similar to hypocalcemia))

Magnesium is important for the body b/c it has what roles?

1. important role in fxn of cell 2. activates enzymes involved in breaking down proteins [[proteins in diet, breaks down carbs, primarily protein breakdown]] 3. helps keep sodium-potassium pump functioning w/in cells [[not adequate Mg = malfunctioning K+/Na+ pump] 4. helps to maintain K+ levels in cells

What happens with dehydration levels? 1. mild 2. moderate 3. severe 4. shock

1. mild = 2% decrease - increased thirst - tears present - mucous membranes moist - extended jugular veins supine - cap refill <2 seconds 2. moderate = 5% - tears decreased - tacky-to-dry mucous membranes - pulse may b elevated - fontanelle may be sunken - oliguria - cap refill time 2-4 seconds 3. severe = 8% - tears = absent - mucous membranes dry - eyes sunken - tachycardia - slow cap refill - poor skin turgor - cool extremities - orthostatic to shocky - apathy - somnolence 4. shock - physiologic decompensation - insufficient perfusion to meet end-organ demand - poor oxygen delivery - decreased blood pressure

Hypermagnesemia nursing management ?

1. monitor VS 2. watch for decreased patellar reflex (deep tendon reflex) 3. neuro changes b/c high Mg = decrease 4. caution pt: OTC meds w/ magnesium in them

How does hyperphosphatemia manifest?

1. neuromuscular irritability & tetany (hypocalcemia) 2. calcified deposition in soft tissue like joints, arteries, skin, kidney & corneas, can cause organ dysfunction <<< monitor organ function

Management of Hypophosphatemia

1. oral supplementation ((bad food)) 2. ingestion of foods high in phosphorus 3. IV administration of sodium or potassium phosphate

When are Isotonic fluids given and why? (referring to NS 0..9%)

1. patient in a code situation b/c it just increases volume NO shift occurs 2. dehydrated or FVD - b/c it replaces the fluid, you're just missing it and you get it 3. hemorrhaging MVA, etc trauma situations - given here

Phosphate does what in the body?

1. primary anion in ICF 2. essential to fxn of muscle, RBCs production & nervous system & muscle system 3. involved in acid-base buffering system, ATP production ((cell fxn, energy)), cellular uptake of glucose, metabolism of (food) carbs, proteins & fats 4. phosphate level HIGH = hypocalcemia hypercalcemia = LOW phosphate level (hypophosphatemia)

What type of situation do we give hypertonic solutions?

1. pt w/ burns 2. low Na+ 3. TPN

What can cause someone to have hypermagnesemia?

1. renal insufficiency 2. dehydration from ketoacidosis - acidosis state from diabetes = high Mg levels 3. addison's disease 4. K+ sparing diuretics (aldosterone) - body holds on to K+, Mg can go up as well 5. excessive use of antiacids & laxatives w/ magnesium EDUCATE here!!!!!! Elderly may use MOM everyday, high Mg levels, and elderly pt may come in and have high Mg levels, just ask and see if thats whats happening (Maalox, Riopan, Milk of Magnesia)

What are the manifestations of FVE in pt?

1. respiratory problems: fluid accumulates in lungs, etc. - SOB, uncomfortable, prefers "up-right position" - "wet lungs" - tachypena --> rales & ronchi present - wet mucous membranes - dependent edema 2. Cardiac issues - BP may be increased, decreased or normal - no postural drop - 3rd heart sound present - resting tachycardia 3. Also... - raised JVD assessed at semi-fowler position, when sitting up J veins are distended - excess IV fluid (post op) - Hx of cardiac failure - confusion, headache, seizures, coma

What are causes of Hyperkalemia?

1. retention of K+ (most COMMON reason is Renal Problems--1st thing you do is look at renal system, usually chronic renal disease) 2. excess release of cellular K+ (like burns, traumatic injury -- cells are crushed in these situations, and the K+ leaks out into ECF) 3. Excess IV/PO K+ (( ex: lethal injections = KCl )) 4. Acidosis or Acidotic patients ((too much acid in system = hyperkalemia )) if you have a pH below 7.35 = hyperkalemic 5. Spirinolactone = K+ SPARING diuretic NOT GIVEN TO SOMEONE W/ RENAL DISEASE OR WHO IS HYPERKALEMIC

Hypocalcemia medical management ?

1. treat underlying cause *** Acute Hypocalcemia = life threatening ** 2. Ca+ replacement - CaCl given slowly IV to prevent cardiac arrest in an emergency situation---on an IV pump VERY SLOWLY 3. respiratory support - can be issues w/ hyperreflexa 4. cardiac monitoring 5. High Ca+ & LOW phosphate diet, includes: green leafy veg, milk products, salmon, sardines 6. Vit D supplements helps us absorb Ca+ 7. antacids<- alot have Ca+ / to decrease elevated phosphorus

Medical Management of Hypernatremia

1. treat underlying cause 2. GRADUAL REDUCTION OF NA w/ fluid replacement 0.2% or 0.45%NaCl or D5W (HYPOTONIC SOLUTIONS) or isotonic 0.9% NaCl --want to avoid sudden shift back into cell 3. diuretic thearpy = Lasix, Furosamide 4. Low Na+ Diet 5. Increased fluid intake (free H2O) = dilute concentrated ECF 6. educate patients, etc 7. monitor neuro stat 8. I&O status 9. Medications w/ sodium | lots of processed & canned foods w/ sodium = teach pt to avoid them 10. watch for oliguria 11. monitor serum Na+ keep w/in normal range

Medical Management of hypomagnesemia

1. tx underlying cause 2. Mg replacement = MgSulfate 3. cardiac monitoring 4. high magnesium diet 5. hypomagnesemia OFTEN accompanied by hypocalcemia --- need to monitor & treat potential hypocalcemia OFTEN low Mg = low Ca+

Hypokalemia : medical management

1. tx underlying cause 2. cardiac monitoring (((first thing))) 3. K+ replacement (try to do through diet, see below) 4. High K+ diet - raisins, bananas, apricots, Oranges, veggies, whole grains, milk, meat, unprocessed, uncooked, sometimes dried fruit 5. unprocessed/uncooked foods = highest 6. aldactone <-- trade name for spirnolactone good to give for hypokalemic pt ************************** spironolactone = increases K+ by stopping excretion of it

Hypercalemia medical mgmt

1. tx underlying cause - chemo for cancer for bone cancer to stop breakdown of bone to stop Ca+ from leaching out into ECF 2. IV NS 0.9% & Lasix == promotes urinary excretion of Ca+ 3. Calcitonin therapy typically IM [calcitonin=helps kidneys excrete Ca+ and decreases bones ability to reabsorb it] 4. low Ca+ diet [dairy products, green leafy veg = DECREASE] 5. bisphosphonates (inhibit osteoclast activity) [stops cells breaking down bone] 6. phosphate therapy [increase phosphate = decrease Ca+ level] 7. aggressive hydration *flush kidney* [IV fluids]

When planning the care of a patient with dehydration, what urine output would the nurse instruct the unlicensed assistive personnel to report?

20 mL for 2 consecutive hours The minimal urine output necessary to maintain kidney function is 30 mL/hr. If the output is less than this for 2 consecutive hours, the nurse should be notified so that additional fluid volume replacement therapy can be instituted.

average healthy adult requires water intake of what per day?

2000-3000 mL - replaces what is lost from body in urinary output & insensible lossess

normal urine output

30 mL / hr if less than this for 2 hours consecutively nurse should be notified so that additional fluid volume replacement can occur

How much fluid is necessary to promote Ca+ excretion?

3000-4000 mL per day | . 3-4 Liters

In someone w/ hypernatremia what is the greatest amount of PO fluid intake that should be given?

700-1900

serum sodium levels *in hypernatremic patients* should not be decreased by more than what? and in what time period?

8-15 mEq in an 8 hour period to avoid rapid shift of water back into cell which could cause cerebral edema & neurological complication

A dehydrated patient is receiving a hypertonic solution. Which assessments must be done to avoid adverse risks associated with these solutions (select all that apply.)?

Blood pressure, lung sounds, and serum sodium levels must be monitored frequently because of the risk for excess intravascular volume with hypertonic solutions.

with HYPOcalcemia what is the role of antacids?

DECREASE elevated phosphorus

Hypokalemia with respect to ICF & ECF

Decrease serum K+ levels increases difference in concentration of K+ between ICF & ECF = reduced excitability of cell so cell = less responsive

Albumin keeps fluid in...

ECF and stay there if not enough ECF = leak out = edema

best indicator for hyperkalemia?

EKG

You are caring for a patient admitted with diabetes mellitus, malnutrition, and a massive GI bleed. In analyzing the morning lab results, the nurse understands that a potassium level of 5.5 mEq/L could be caused by which factors in this patient (select all that apply.)?

Hyperkalemia may result from hyperglycemia, renal insufficiency, or cell death. Diabetes mellitus, along with the stress of hospitalization and illness, can lead to hyperglycemia. Renal insufficiency is a complication of diabetes. Because malnutrition does not cause sodium excretion accompanied by potassium retention, it is not a contributing factor to this patient's potassium level. Stored hemolyzed blood can cause hyperkalemia when large amounts are transfused rapidly. The patient with a massive GI bleed would have an nasogastric tube and not be eating. The potassium level may be increased if the patient has nephropathy. There may be excess potassium being released into the blood as a result of massive blood transfusion. The potassium level may be increased because of dehydration that accompanies high blood glucose levels.

Hypocalcemia does what as far as excitability?

INCREASES

What is an important risk factor a patient may have that prevents the nurse from giving Lactated Ringers? Why does this matter?

Liver Diseases from : -Chronic Alcoholism - Cirrhosis - hepatic disease Liver breaks down the lactate in lactated ringers and without proper liver functioning lactate can accumulate in the body = BAD

You are admitting a patient with complaints of abdominal pain, nausea, and vomiting. A proximal bowel obstruction is suspected. Which acid-base imbalance do you anticipate in this patient?

Metabolic alkalosis Because gastric secretions are rich in HCl acid, the patient who is vomiting will lose a significant amount of gastric acid and be at an increased risk for metabolic alkalosis.

What to know about K administration

NEVER IM NEVER push or bolus NEVER add KCl to hanging IV bag to prevnt giving a bolus dose if you DONT see pee you DONT GIVE K always in 1 L or 1000 mL of something else always w/ infusion pump always mix IV bag to distribute K+ always assess IV site for phlebitis/infiltration rates on pump should NEVER exceed 10 mEq/hr UNLESS pt is in critical care setting w/ continuous ECG & central line access for admin. usually ONLY given if urine output is 0.5 mL/kg of body weight per hour

If Ca+ is high what do we give?

NS 0.9% and lasix calcitonin to decrease GI absorption, increase renal secretion and to deposit Ca+ in bone (typically IM injection) bisphosphonates which inhibit osteoclast activity (bone doesnt get broken down = less ca+ released to body) phosphate therapy b/c Ca+ & phosphates are inversely related high Ca+ = LOW phosphate agressive fluid intake for flushing kidneys

What regulates Na+?

Na+ intake: PO (diet), Meds, IV admin Aldosterone: made in adrenal glands which increases Na+ reabsorption which means if you have a problem w/ adrenal glands = affects Na+ ((adosterone = increases reabsorption of sodium)) also -- kidneys excrete Na+ so problem w/ renal failure = problem w/ Na+ excretion ALSO remember that when we reabsorb Na+ we're going to lose K+ through kidney, sodium-potassium pump = why thats true

note that Ca has relationships w/

PO4 & pH if Ca is low then PO4 is HIGH pH is HIGH

hyperkalemia EKG

Peaked T waves and widened QRS.

What are the major Cation & Anion of ICF?

Potassium Posphate HPO4-3 sodium potassium pump?

You receive a physician's order to change a patient's IV from D5½ NS with 40 mEq KCl/L to D5NS with 20 mEq KCl/L. Which serum laboratory values on this same patient best support the rationale for this IV order change?

Sodium, 135 mEq/L; potassium, 4.5 mEq/L The normal range for serum sodium is 135 to 145 mEq/L, and the normal range for potassium is 3.5 to 5.0 mEq/L. The change in the IV order decreases the amount of potassium and increases the amount of sodium. Therefore, for this order to be appropriate, the potassium level must be near the high end and the sodium level near the low end of their respective ranges.

K+ sparing diuretic

Spironolactone (we keep it)

When assessing a patient admitted with nausea and vomiting, which finding best supports the nursing diagnosis of deficient fluid volume?

Restlessness is an early cerebral sign that dehydration has progressed to the point where an intracellular fluid shift is occurring. If the dehydration is left untreated, cerebral signs could progress to confusion and later coma

While caring for a patient with metastatic bone cancer, which clinical manifestations would alert the nurse to the possibility of hypercalcemia in this patient (select all that apply.)?

Signs of hypercalcemia are lethargy, fatigue, weakness, depressed reflexes, muscle flaccidity, heart block, anorexia, nausea, and vomiting. Paresthesia, facial spasms, and muscle tremors are symptoms of hypocalcemia.

What are the major Cations & Anions in ECF?

Sodium Chloride *** know values see separate chart of values

EKG hypokalemia

U wave - delayed repolarization of ventricles Flattened T wave

What are the two most common reasons for FVD?

Vomiting & Diarrhea

What happens in Hyponatremia w/ ICF / ECF?

Water shifts to cells cells swell ECF= dilute, not concentrated

What does maintenance of phosphate require ?

adequate renal functioning

nursing mgmt for hypercalcemia

admin meds as ordered ekg changes (everything slows) monitor bowel sounds q 8 hrs

Manifestations of Hypoklemia

anorexia, nausea, vomiting (from ileus r/t SLOWED smooth muscle contraction) muscle weakness, leg cramps, paralysis EKG changes (FLATTENED T wave & ELEVATED U WAVE)---- cardiac issues--> conduction is decreased, excitability is decreased parathesias (numbness & tingling) polyuria & thirst if low K+ is prolonged ^^^^ pt w/ N+V they start becoming dehydrated slow, weak pulse, shallow respiration, confusion, depression, fatigue, lethargy K+ less than 3.5 mEq/L -----GI bug how do you feel when you've had that, keep this in mind to remember these----

Fluid Volume Excess labs

decreased BUN decreased Sodium decreased HH decreased plasma osmol decreased urine osmol

What type of patient receives hypotonic fluids?

dehydrated patients

with hypercalcemia you need to FIRST

begin by hydrating the patient w/ IV isotonic saline *0.9%* to maintain a urine output of 100-150 mL per hour ***monitor for fluid overload due to impaired renal fxn

Metabolic Acidosis

can cause HYPERCALCEMIA

Metabolic ALKALOSIS

can cause HYPOCALCEMIA

Hypocalcemia and ICF/ECF

capillary permeability is increased which leads to increased neuromuscular excitability hyperactive motor & sensory nerves bone loss occurs as Ca is pulled from bone to compensate [ body wants homeostasis in ECF ]

Why confusion in LOW & HIGH sodium pt?

cell experiences a fluid shift both ways, either swelling or shrinking especially brain cells

What happens to cells w/ hypertonic fluids?

cell shrinks, shrivels fluid leaves cell into vascular space

with hyponatremia we need to observe patients for (having to do w/ volume of fluids)

circulatory overload s/s of increasing - SOB, HR, RR

Hyponatremia medical management

hyponatremia from too much water then.....Mild Hyponatremia = water restriction ------*****---- water restriction to 500 mL LESS thn the previous 24 hour urine output -----******------ ex: pt put out 1000 mL day before THEN the next day the patient is ONLY allowed 500 mL Acute/Serious Hyponatremia = slow increase in Na+ to prevent neuro damage administer 3%-5% Na+ solutions (((use caution)))) (hypertonic solutions)

Fluid Volume Deficit labs

increased BUN increased Na+ increased HH increased plasma increased urine osmolality

Ca has what relationship w/ PO4

inverse high Ca+ = LOW po4 high po4 = LOW ca+

What type of relationship is their between Calcium& phosphate?

inverse aka reciprocal

What do nurses monitor in patients receiving hypotonic solutions?

monitor neuro function are they getting confused, lethargic, basic mental status

What should be monitored in the patient when administering hypertonic fluids?

neuro checks

What patient should NEVER get D5?

neuro patient, post op brain surgery, head trauma b/c hypotonic fluid = cell swelling = increased brain swelling = BAD news

Potassium does what in the body?

neuromuscular excitability muscle contraction ((((especially the heart)))) (((neurosystem too))) acid-base balance (exchanges w/ H+)

What controls serum levels of phosphate?

parathyroid gland hormone

hypophosphatemia can be caused by? ((think about TUMs, etc)

phosphate binding antacids

Foods where Potassium is found

proteins, vegs, fruit, whole grains, uncooked/raw & unprocessed foods healthy milk, apricots, bananas, oranges, meats, whole grains

How often do we monitor bowel sounds in hypercalcemia?

q 8 hr

Why circulatory overload in hyponatremia patients?

replacing sodium back in, which puts them at risk for circulatory overload, especially pt on hypertonic solutions, theres a risk of a large fluid shift, need to be monitored for increased SOB, HR, RR <<< fluid overload

what type of diuretic is okay to give to someone who is hypokalemic?

spirnolactone

with HYPERNATREMIA

the bowels will be hypoactive

Why is hypernatremia not very common?

thirst mechanism

What type of situation do we give LR (lactated ringers)?

trauma