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FLUID AND ELECTROLYTES

Terms in this set (88)

Potassium
Major INTRACELLULAR electrolyte
Important in cardiac and skeletal muscle activity
Regulated by the kidneys
Aldosterone increases excretion of K+
Normal range
3.5-5.0 mEq/L
Hypokalemia
<3.5 mEq/L
Will happen b/c:
-deficit in total K+ stores
-a shift of K+ into the cell (i.e. alkalosis)
Causes
K+ wasting diuretics
GI loss (diarrhea etc.)
Alkalosis- K+--> into cell, H+--> out of cell to balance pH
HyPERaldosteronism- Increases renal K+ wasting
Insulin causes K+ to move into cell (monitor pt.'s receiving high carbohydrate IV nutrition)
Poor intake- elderly, alcoholics, bulimics etc.
S/S
Less Action Potential
decreased bowel motility
Muscle weakness, leg cramps
Dysrhythmias- ventricle fib- extremely low K+, need to be on cardiac monitor (EKG)
A SIC WALT *
A-alkalosis
S-shallow respirations
I-irritability
C-confusion, drowsiness
W-weakness, fatigue
A-arrhythmias- irregular rate, tachycardia
L-lethargy
T-thready pulse
* decreased intestinal motility, N/V, ileus
Medical management
Dietary, oral or IV, replacement
Foods high in K+
Salt substitutes
IV KCl, Kphos, K acetate
Nursing management
Correct K+
Monitor ECG
Careful I/O monitoring
Monitor for digitalis toxicity (low K+ will put digoxin pt.'s into toxicity)
Pt. education: laxatives, diuretics, intake
Mild to moderate-oral supplements
Severe, unable PO-IV- Have to have adequate urine flow before beginning therapy
Never IV push or IM, always IV infusion pump
Hyperkalemia
>5.0 mEq/L
Extremely dangerous at risk for cardiac arrest
When it will happen: Pt.'s with impaired renal function-unable to excrete K+ Often treatment induced
Causes
-Decreased renal excretion
-Rapid administration of K+
-Movement of K+ from ICF to EFC (acidosis)
-HyPOaldosteronism- excretes Na and retains K+
-Medications: KCl, K+ sparing diuretics, ACE inhibitors
-Excessive stored blood administration
-Extensive tissue trauma- burns
More Action potential
S/S
-Dysrhythmias: Peaked, narrow (real tall)
T waves-maybe first sign
-Tachycardia that leads to bradycardia
-Skeletal muscle weakness
-GI: intestinal colic, cramps, distention
Medical management
-ECG
-Serum K+ redraw to confirm
-Restrict dietary K+ and salt substitutes
-Kayexalate- PO or enema; binds with K+ in GI tract for elimination
Emergency management
-IV calcium gluconate: antagonizes action of K+ on heart muscle--does not reduce serum K+
-IV sodium bicarbonate: alkalinize plasma to cause temp. shift of K+ into the cell
-IV regular insulin and IV D50: temp. shift into cell
-These start working within 30 mins
-IV lasix: renal excretion of K+
-Peritoneal or hemodialysis
Nursing management
-Monitor at risk pt.'s
-Renal failure
-Encourage adherence to renal diet (low K+)
-Closely monitor K+ solutions/infusions
-Observe for S/S of muscle weakness and dysrhythmias
Role of sodium:
-Major: controlling water distribution-Est. electrochemical state for muscle contraction and transmission of nerve impulses
Normal range:
135-145 mEq/L (most abundant in ECF)
Regulated by:
ADH, thirst ,renin-angiotensin-aldosterone system
Hyponatremia:
<135; <118 is critical -Usually due to water imbalance
Causes:
-Vomiting, diarrhea, sweating-Diuretic use-Adrenal insufficiency, aldosterone deficiency -Medications(anticonvulsants, SSRI's) -SIADH (swimming in ADH) skin loss, BURNS
S/S:
-NEURO CHANGES: H/A, seizures, AMS, coma-from cellular swelling and cerebral edema
-N/V, anorexia
-Decreased urine specific gravity->115 mEq/L: Increased ICP(Intracranial pressure)
- letharrgy, confusion, muscle twitching, weakness, seizures
EKG CHAGES
SEIZURES
Diagnostics:
Neuro assessment Identify the cause serum sodium, osmolality, urine specific gravityMedical management: Water restriction (safest) Na replacement (high concentrations in ICU only)
Nursing management:
provide fluid monitor LOC- seizure precautions monitor serial serum sodium
Medical management:
Hypertonic solution 0.33% or 0.45% NSD5W infusiondiuretics -Give A LOT of volume first Reduce Na levels SLOWLY to avoid cerebral edema DDAVP (synthetic ADH) for diabetes insipidus
Water restriction (safest)
Hypernatremia:
>145 mEq/L
Causes:
-Fluid deprivation in unconscious
-very old, very young, or cognitively impaired
-hypertonic enteral feedings w/o water supplement
-watery diarrhea-insensible losses: burns, hyperventilation
-diabetes insipidus
-heat stroke, sea water, malfunction of dialysis, IV hypertonic saline, excessive sodium bicarbonate
EKG AND SEIZURES, THRIST
S/S:
THINK NEUROLOGIC (water is moving out of cells causing them to shrivel)
-restlessness, irritability, disorientation, delusions, hallucinations
-permanent brain damage if severe enough- hemorrhages from brain contraction-thirst, dry/swollen tongue, sticky mucous membranes-increased muscle tone and DTR's -flushed skin
Diagnostics:
increased serum sodium increased serum osmolality (>300) and urine specific gravity (kidneys are trying to hold onto water)-Unless the cause is diabetes insipidus, then the water will be dilute
Nursing management:
I/O and daily weights monitor LOC monitor serum sodium enforce fluid restriction- educate pt. and family
Medical management:
hypotonice, ISOTONIC SOLUTION Iv D5W .9% NS lactated ringers
Magnesium:
-Found in bone and soft tissues
-Excreted by the kidneys -Activator for intracellular enzyme systems
-Plays role in carbohydrate & protein metabolism
-Variations affect neuromuscular irritability and contractility
Magnesium produces:
-Sedative effect at neuromuscular junction
- inhibits release of acetylcholine (hypercalcemia also) -Peripheral vasodilation
Normal range:
1.5-2.5 mg/dL
Hypomagnesemia:
<1.5 mg/dL Assoc. with hypokalemia and hypocalcemia
Causes:
-GI loss-Any disruption in small bowel function
-ETOH withdrawal-most common--mag moves inside cell with IV glucose administration
-During nutritional replacement
-Meds-DKA: osmotic diuresis & mag shifts into cell w/ insulin therapy
S/S:
More Action Potential
-Tremors-Athetoid movements: slow, involuntary twisting and writhing
-S/S assoc. with hypocalcemia-usually accompanying (tetany, seizures, laryngeal, Hyperactive DRTs)
confusion
MIMICS HYPO CALCIMINE
chvostek , trousseau signs
Medical management:
-Dietary: green leafy veggies, nuts, seeds, legumes, whole grains, seafood, peanut butter,cocoa-Oral supplements-IV supplements by IV infusion pump
Nursing management:
dysphagia screening (diffculty swallowing; at risk for aspirations)
-Pt. education: overuse of laxatives-Refer to counseling, support, ETOH programs
Hypermagnesemia:
Rare >2.5 mg/dL
Causes:
-Renal failure
-Excess mag administration (-Excess use of Mag containing antacids or laxatives
-Adrenocortical insufficiency,
Addison's disease
- trauma, burns, shock, sepsis, cardiac arrest
S/S:
-CNS depression (same as ^ Ca2+)-Peripheral vasodilation (lowered BP)-Muscle weakness-facial flushing, sensations of warmth (b/c of vasodilation)-lethargy, dysarthria, drowsiness-Loss of DTR's, muscle weakness, paralysis-depressed resp. center-coma, AV heart blocks, cardiac arrest
MIMIC HYPER CALCIMINE
hypo-active DTRs
Medical management:
-Emergency: ventilatory support and IV calcium gluconate (antagonizes CV and NM effects of mag)-Lasix and NS infusion-Dialysis
Nursing management:
-Assess at risk pt.'s for resp. depression and hypotension-Assess LOC and DTR's -Avoid mag containing meds Promoting URINATION, IV Calcium
Calcium:
-99% in skeletal system (bones and teeth)
-Major in transmitting nerve impulses
-Helps regulate muscle contraction & relaxation (heart too)
-Role in blood coagulation-Absorbed from food in presence of normal gastric activity and Vit. D
Inverse relationship with PHOSHORUS
regulated by PARATYROID
Normal range:
8.6-10.2 mg/dl
Serum Ca2+
controlled by: PTH and calcitonin
Low serum
Ca2+: parathyroid-->PTH-->increased Ca2+ absorption from GI, reabsorption from renal tubule, release Ca2+ from bone
High serum Ca2+:
Thyroid-->calcitonin-->inhibits Ca2+ reabsorption from bone-->decreases serum Ca2+ concentration. Calcitonin keeps the tone in the bone--keeps Ca2+ in bone (inhibits release)
Hypocalcemia:
<8.6 mg/dL
Causes:
More Action Potential
-Hypoparathyroidism (surgical or primary)
-Elevated Phosphorus, Mg down , VitD down
-Pancreatitis (results in secretion of calcitonin)
-low serum albumin
-Alkalosis (calcium will bind with proteins)
S/S:
-Tetany (spasms) -Tingling in fingers, around mouth, feet
-Hyperactive DTR's
-Trousseau's sign
-Chvostek's sign
-Mental changes (depression, impaired memory, confusion, delirium, hallucinations)
-Prolonged QT -Impaired clotting -Osteoporosis: with prolonged deficit
Chvostek's sign:
Spasms of the facial muscles produced by sharply tapping over the facial nerve in front of the parotid gland and anterior to the ear; late sign of tetany
Trousseau's sign:
Is positive when carpopedal spasm is induced by occluding blood flow to the arm for 3 minutes with a blood pressure cuff; late sign of tetany
Nursing management:
-Monitor airway for laryngeal stridor -Safety precautions (if mental changes occur) -IV administration: monitor site for extravasation that can cause cellulitis or tissue necrosis -Pt. edu: Ca2+ rich foods -ETOH and caffeine inhibit absorption-Cigarettes increase urinary excretion -Avoid overuse of antacids and laxatives containing phosphorus
Medical management:
-Acute symptomatic: IV administration of calcium gluconate or calcium chloride -Vit. D therapy to increase absorption from GI tract -CRF pt.'s: aluminum hydroxide, Calcium acetate, calcium carbonate antacids to decrease elevated phosphorus -Increase Ca2+ intake: milk, green leafy veggies, canned salmon, sardines, oysters. NEVER give CA IM
Medical management:
Give Diaretics and increase fluids and Hydrate
Causes:
Low Action Potential
-Malignancies -Hyperparathyroidism
-Excess PTH secretion causes increased renal and GI absorption of Ca2+ and increased release from bones
-Can lead to calcification of soft tissue -Immobility-causes bone mineral to be lost in bloodstream
-Meds: thiazides, calcium carbonate antacids, Vit. A and D intoxication, chronic lithium use, theophylline toxicity
Hypercalcemia:
>10.2 mg/dL -50% mortality rate if not treated promptly -Cardiac standstill at approx. 18 mg/dL
S/S:
-Muscle weakness, decreased DTR's -Anorexia, N/V, constipation -Abd. and bone pain -Abd. distention, paralytic ileus -Fractures -Bone Pain
EKG changes
Diagnosed:
-Serum Ca2+ -ECG monitoring
Nursing management:
-Encourage ambulation (Ca2+ back into bone) and fluids -Encourage fiber intake (helps with PUD) -Safety precautions -Monitor ECG
Phosphorus: Essential in:
-function of muscle and RBC's
-formation of ATP
-Maintenance of acid-base balance, the nervous system, carb, protein, and fat metabolism
-structural support of bones and teeth
Normal range:
2.8-4.5 mg/dL 85% in bones and teeth primary anion in ICF
Hypophosphatemia:
<2.8 mg/dL -Most common in re-feeding after starvation (same as decreased mag)
Causes:
DKA -Re-feeding after starvation-anorexia nervosa, alcoholism, elderly debilitated unable to eat-TPN-ETOH withdrawal (same as decreased mag)
-Poor intake
-Excess phosphorus binding by antacids
Respiratory Alkalosis
RENAL FAILURE
S/S:
-S/S of hypercalcemia: ATP deficiency: irritability, fatigue, weakness, apprehension, numbness, paresthesias confusion,
Muscle weakness, pain; acute
cardiac dysthmiasa
RENEAL FAILURE
osteomalacia
Medical management:
-Prevention-Adequate amounts added to TPN and enteral solutions
-Oral supplements
dairy products
Nursing management:
-Severely malnourished: start TPN slowly to avoid massive shift of phos. into cell-Infection prevention (granulocyte alterations)-Assess LOC-Diet: milk, milk products, organ meats, nuts, fish, poultry, whole grains-Meds: Neutra Phos capsules, KPhos, Fleet's Phospho-Soda
Hyperphosphatemia:
>4.5 mg/dL
Causes:
-Renal failure-Increased intake, decreased output-shift from IC for EC-TPN-Acute hemolysis-Profound muscle necrosis-Primary complication: metastatic calcification (soft tissues, joints, arteries)
S/S:
RENAL FAILURE (S/S of hypocalcemia)-Tetany, anorexia, N/V, bone and joint pain, hyperreflexia, tachycardia, muscle weakness decreased calcium restrict diary.
Medical treatment:
-Treat the cause -Ampho jel w/ meals to bind phos.-Forced diuresis w/diuretics-HD (dialysis)-Surgery to remove Ca2+ deposits
Nursing management:
-Avoid phosphorus rich foods:-hard cheeses, nuts, meats, whole grains, dried fruits and veggies, sardines, sweetbreads, foods w/milk-Avoid phos. containing laxatives
Hypovolemia:
Loss of ECF
Causes:
prolonged inadequate intake vomiting, diarrhea, GI suctioning sweating third space shifts diabetes insipidus, adrenal insufficiency osmotic diuresis hemorrhage
S/S:
Acute weight loss decreased skin turgor oliguria (decreased urine output); concentrated urine weak, rapid HB increased thirst cool, clammy, pale skin anorexia, nausea, muscle weakness, cramps
Diagnosed:
BUN: Creatinine ratio >20:1 Elevated hematocrit
Assessment:
H&P to identify cause
Medical treatment:
Mild to moderate: oral route preferred if able to drink Sever: IV replacement with Isotonic initially to expand plasma volume --Possible fluid challenge to assess kidney function and response
Nursing management:
Strict I/O Daily weights monitor VS skin turgor and mucous membrane assessmentLOC
Hypervolemia:
Abnormal retention of water and sodium in ECF
Causes:
Simple fluid overload Diminished function of homeostatic mechanisms:--HF--Renal failure--Cirrhosis Excess salt intake (oral or IV)
S/S:
Edema distended neck veins crackles (pulmonary edema) tachycardia, increased BP increased weight increased urine output SOB, wheezing
Diagnosed:
Decreased BUN and hematocrit (due to plasma dilution)--possible pulmonary congestion on CXR
Medical management:
Treat the cause----turn off NS* diuretics restricting fluids and Na
Diuretics:
Inhibit reabsorption of Na and water by kidneys --mild to moderate: thiazides--severe: loop--S/E: hypokalemia hyponatremia hypomagnesemia --may need electrolyte replacement
Dialysis:
Hemo or peritoneal removes nitrogenous wastes controls potassium controls acid-base balance removes sodium and fluid --low sodium diet (2gm/day or less)
Nursing management:
Strict I/O, daily weights assess breath soundsassess for dependent edema
Prevention:
promote rest, restrict Na intake monitor IV fluid intake and response turn pt. and check skin **Pt. education
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