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what are electrolytes?
essential ions found in the body
positively charged (+, cation)
negatively charged (-, anion)
cations
positive charge
ex)
Na+
K+
Ca+2
Mg+2
anions
negative charge
ex)
chloride:Cl-
bicarbonate: HCO3-
phosphate: PO4-3
sulfate: SO4-2
functions of electrolytes
nerve conduction
muscle function
fluid balance
acid-base balance
cellular function
normal Na+ lab values
135 - 145 mEq/L
normal Cl- lab values
98 - 106 mEq/L
normal K+ lab values
3.5 - 5.0 mEq/L
normal Ca+2 lab values
9.0 - 10.5 mEq/L
normal Mg+ lab values
1.3 - 2.1 mEq/L
normal PO4-3 lab values
3 - 4.5 mg/dL
Na+ functions
normal range: 135 - 145 mEq/L
influences fluid distribution
influences blood pressure
acid-base balance
muscle contraction
nerve impulse transmission
regulated by kidneys
nutrient transport
Cl- functions
normal range: 98 - 106 mEq/L
direct relationship with Na+
nerve conduction
acid-base balance
lost in sweat
part of stomach acid, pancreatic enzymes
nutrient transport
dietary intake - Na+
higher sodium
processed foods
preserved foods
cheese
dried meats
canned foods (not fruits)
lower sodium
fresh/frozen veggies and fruits
dried druits
canned fruit
rice, pasta
unsweetened oatmeal
fish, shellfish
fat-free/low-fat milk & yogurt
hypernatremia
serum sodium: >145 mEq/L
losing water → sodium is now more conc in the blood
or gaining more sodium than water → hypertonic fluid IV or eating crazy sodium
water shifting into the bloodstream and out of cells → sodium more concentrated in the blood → cells shrink
patients at risk for hypernatremia
Na+ retention
hyper-aldosteronism → aldosterone incr sodium/water retention
cushing’s
uncontrolled diabetes mellitus
Na+ intake
lots of dietary Na+
corticosteroids → incr sodium/water rentention
IV fluids
hypertonic tube feedings w/o free H2O
water loss
H2O deprivation
increased insensible water loss (fever)
diarrhea
diabetes insipidus (DI) → peeing out body’s volume
inadequate water intake
elderly
infants
comatose pts
pts with cognitive dysfunction
hypernatremia: assessment findings
extremely rapid shift/extremely high Na+
brain cell shrinkage
vascular rupture
cerebral bleeding
neurological damage
death
increased Na+ = thirst
CNS signs → confusion, restless, agitation, seizures, coma, death
hypovolemic hypernatremia
see this w dehydrated ppl → see neurosymptoms and hypovolemia symptoms
tachycardia
decreased BP
dry mucous membranes
hypervolemic hypernatremia
see neuro symptoms + hypervolemia symptoms
weight gain
peripheral/pulmonary edema
increased BP
increased JVD
hypernatremia: interventions
hypovolemic
NS or LR until hypovolemia improves
provider will calculate H2O deficit
if necessary, then admin hypotonic fluid (1/2 NS, D5W, or PO H2O) to replace fluid deficit
rehydrate them by giving fluids
euvolemic
provider will calculate H2O deficit
adminster hypotonic fluid (1/2 NS, D5W, or H2O) to replace water deficit
give hypotonic fluid bc that will balance sodium level faster without adding too much volume
hypervolemic
free water replacement (D5W) + loop diuretics
hemodialysis if renal failure
dietary
restrict Na+
meds
diuretics
no meds that contain sodium
monitor
physical assessment findings
Is & Os
daily weights
labs: HCT, glucose, electrolytes
comfort
mouth, lip care
alcohol-free mouthwash
skin care
education
teach abt sodium in foods (<2000 mg/day)
OTC meds that contain Na+ should be stopped
body positioning if FVE
hyponatremia
serum sodium <135 mEq/L
losing more sodium than water
higher concentration of sodium in the cells than in vasculature
water moves into cells → cells swell → BAD in brain cells
cerebral edema → serizures + confusion
patients at risk for hyponatremia
increased water
syndrome of inappropriate ADH secretion (SIADH)
increased ADH → body holds onto more water
CHF
psychogenic polydipsia
increased Na+ loss
renal loss
GI loss
NG suctioning
skin loss
wound damage
severe burns
hormonal
hypoaldosteronism → body doesn’t retain as much sodium anymore (uncommon)
decreased dietary Na+ intake
rare
extreme hyponatremia
serum sodium: <120 mEq/L
patient might be suddenly very confused when they were not before → check their sodium level
acute cases: brain swelling is big concern
signs of hyponatremic encephalopathy
lethargy
headache
restlessness
disorientation
seizures, coma, death
anorexia
nausea & vomiting
muscle cramps
weakness
weak/absent DTRs
hyponatremia assessment findings
neuro
cerebral edema → headache
confusion
headache
MS
decreased muscle tone
weakness
decreased DTRs
fatigue
CV
increased HR
increased JVD if hypovolemia
postural hypotension
GI
increased motility
cramping
nausea/vomiting
respiratory
severe muscle weakness can inhibit respiratory functions
labs
na+ , cl - will be decreased
increased serum osmolality
increased HCT
hyponatremia interventions
monitor
I & O
labs
daily weights
LOC
potential for seizures if severe
fluids
hypovolemia: IVF/PO - w Na+ replacement → 0.9% NaCl
euvolemia: treat cause, no additional fluids needed
hypervolemia: restrict fluids if delusional or too much intake
severe/rapid onset w lots of symptoms: 3% NS slowly
prevent major risks w correcting sodium too fast
brain cells are super sensitive to fluid shifts
other
prevent further decline in serum na+
reorient
safety interventions
educate pt and family
hypertonic NaCl safety
3% or 5% NaCl IV
restrict to CCU/ICU/ED
never override drug dispensing machine to obtain the med
use smart pump alerts for proper rate guidelines
central line recommended
monitor Na+ q6h
monitor for possible side effects
elevated intracranial pressure (ICP), renal impairment, subarachnoid hemorrhage (SAH), natriuresis, increased urine output (UOP)
program rate as prescribed
too-rapid rate can cause osmotic demyelination syndrome
permanent brain damage
be careful in bringing Na+ level down and up
can’t be too quick or too aggressive
strip myelin off of nervous cells → irreversible damage to the brain
potassium normal serum level
3.5 - 5.0 mEq/L
potassium functions
correlates frequently with Na+ (opposing), but not direct relationship
important in cardiac and muscle function
too much or too little causes arrythmias
maintaining electrolyte balance
nerve function
muscle function
cramping
heart function
arryhthmias
acid-base balance
kidney function
cellular metabolism
**K+ plays big role in depolarization of muscle
dietary intake - K+
higher K+
dried fruit
spinach
beef
chocolate
pork
tomatoes
potatoes
bananas
lower K+
eggs
bread
cherries
apples
peaches
cauliflower
celery
green beans
peppers
peas
hyperkalemia serum levels
serum potassium: >5 mEq/L
hyperkalemia patients at risk
decreased excretion → bc renal failure
decreased aldosterone → bc adrenal insufficiency/addison’s disease
potassium-sparing diuretic → spironolactone
K+ shift → excessive exercise, cell injury, catabolism, diabetes mellitus, medications
other→ salt substitutes, digoxin, beta-blockers
hyperkalemia: asssessment
GI
nausea/vomiting
abdominal cramping
diarrhea
cardiac
tall, peaked T-waves
widening QRS
deadly arrhythmias
mental
irritability (not confusion)
anxiety
fatigue
neuromuscular
paresthesia
weakness
muscle cramping
hyperkalemia: ECG changes
tachycardia → bradycardia
possible cardiac arrest
tall, tented T waves
hyperkalemia: interventions
eliminate K+ intake → no salt subtitutes
increased K+ elimination → loop diuretics, SODIUM POLYSTYRENE SULFONATE
promotes GI excretion of potassium in stool
force K+ out of ECF into ICF
insulin + glucose
insulin lowers blood sugar by moving sugar into cells
glucose goes into cells but K+ does too
K+ levels decrease because it moved inside the cells
give insulin IV to lower K+ levels → BUT ALSO GIVE GLUCOSE bc we made glucose also move inside the cells → prevent hypoglycemia
protect the heart
10% calcium gluconate IV
dialysis if renal failure
monitor: ECG, labs, bowel sounds, stool, muscle strength
educate: diuretic use, muscle weakness, avoid K+ rich foods, safety
hypokalemia serum level
serum K+: <3.5 mEq/L
hypokalemia: patients at risk
renal
hypoaldosteronism
skin
excessive diaphoresis
GI
vomiting, diarrhea, NG suctioning, poor PO intake
meds
K+ wasting meds → furosemide
corticosteroids → prednisone… in hyperaldosterone, high levels of steroids in body.. steroid hormones cause elevated blood sugar → increase insulin production. K+ goes into cell as a result along with glucose.
conditions/medications that cause elevated cortisol or blood sugar will result in hypokalemia → K+ moving inside cells
laxative overuse
excessive insulin
hypokalemia assessment
CV
prominent U waves
S-T depression
prolonged QRS
MS
weakness, parethesia
decreased smooth muscle function
neuro
decreased DTRs
depression
confusion
GI
decreased gastrointestinal motility
paralytic ileus
respiratory
shallow respirations
miscellaneous
hyperglycemia
fatigue
hypokalemia: ECG changes
prominent U wave
S-T depression
prolonged QRS → causes ventricular arrhythmias → deadly
hypokalemia: interventions
hydrate to maintain urine output of <0.5 mL/kg/hrHydrate
supplement oral: replace K+ in diet or supplements
supplement IV:
no more than 10-20 mEq/hr by IV pump
GIVE 10 MEQ/HR by IV PIGGYBACK → if give too quick, cause cardiac arrhythmias
NEVER GIVE K+ IV PUSH → WILL KILL PT
monitor: ECG, vitals, respiratory status, BS
other: treat constipation, hold K+ wasting diuretics, consider changing diuretic class change
education: S/S hypokalemia, laxative overuse, safety, S/S orthostatic hypotension
Ca+2 normal serum levels
serum level: 9 - 10.5 mEq/L
calcium functions
required for clotting
needed for muscle contractions
used in enzyme activity
assists with nerve impulses
important for strength and durability of bones/teeth
what is Ca+2 absorption influenced by
active vitamin D (calcitrol/sunlight) required for GI absorption
PTH → increased serum Ca+2
PTH releases Ca+2 and signals kidneys to activate vitamin D → GI tract will absorb more Ca+2
INCR PTH = INCR CA+2
INCR calcitonin = DECR Ca+2
Ca+2 and phosphate have an inverse relationship
when body detects high Ca+2 → stop producing PTH and instead secrete calcitonin
calcitonin tells bones to absorb calcium bc too much in blood and tells kidneys to not secerete vitamin D. also tells gut to not absorb calcium
CALCIUM CALMS
dietary intake Ca+2
higher in Ca+2
almonds
antacids
creamed soups
molasses
sardines
turnip greens
spinach
lower in Ca+2
fruits
beans
carrots
radishes
hypercalcemia serum concentration
serum calcium > 10.5 mEq/dL
patients at risk for hypercalcemia
RHINO
Renal Insufficiency
cannot decrease Ca+2 through kidneys
Hyperparathyroidism
parathyroid hormone is overactive
too much PTH = too much Ca+2 absorbtion
Immobilization
reduced mechanical loading on bones → calcium leaks out of bones
Neoplasms
cancer
bone metastasis → cancer eats away at bones and bone contents release
Other endocrineopathies
issues w thyroid → impact parathyroid
hypercalcemia assessment
neuro
LOC changes
confusion
depression
lethargy
GI
decreased peristalsis
constipation
abdominal discomfort
MS
weakness
fatigue, lethargy
decreased DTRs
bone pain
GU
kidney stones
polyuria
dehydration
CV
decreased HR
DVT risk
heart block
postural hypotension
ECG changes → shortened S-T
hypercalcemia interventions
hydration
3-4 L daily → decreases risk of calcium stones → flush it thru
promote excretion
IV NS → match rate up to UOP
loop diuretics
reduce serum Ca+2
calcitonin → inhibits bone breakdown
avoid Ca+2 containg meds
calcimimetics to regulate PTH
inhibit bone loss of Ca+2
weight-bearing activities
bisphosphonates → decrease calcium release from bones by inhibiting osteoclasts
safety/monitor
protect against fractures
ambulation
fall risk
telemetry
monitor VS, labs
other
strain urine (stones)
Tx constipation, nausea
decreased dietary intake of Ca+2
dialysis → if kidneys aren’t working at all
correct underlying cause
no thiazide diuretics
hypocalcemia serum level
serum Ca+2: <9 mg/dL
start seeing effects when less than 7 mg/dL
patients at risk for hypocalcemia
inadequate Ca+2 intake
inadequate absorption
ETOH → ethanol alcohol
vitamin D deficiency → not absorbing Ca+2
Ca+2 excretion
diuretics
anticonvulsants
calcitonin
laxatives
other
increased dietary phosphate
decreased PTH
calcium deposits in bone, tissue
blood transfusions
memory trick for patients at risk of hypocalcemia
DAILY PIC CAD
diuretics
alcohol
inadequate intake/absorption
laxatives
yielded photphate increase
pth decreased
iv blood transfusions
calcitonin
calcium depots in bone/tissue
anticonvulsants
vitamin D deficiency
hypocalcemia assessment → mild to moderate
NEURO SYMPTOMS: CATT (mild to moderate) HILLS (severe)
Confusion
Anxiety
Tremors & palpitations
Tingling & numbness in hands, toes, and lips
CV
palpitations
Miscellaneous
muscle cramping
fatigue
weakness
brittle nails, hair loss
hypocalcemia assessment → severe
NEURO SYMPTOMS: CATT (mild to moderate) HILLS (severe)
Hyperreflexia → big DTR reaction reflex
Irritability
LOC changes → delirium, non-responsiveness
Laryngospasm & stridor
not enough Ca+2 can cause muscle excitability
bad if have spasm in larynx bc can close airway and cause stridor
Seizures & tetany
overexcitability → missing calm component
CV
impaired clotting
hypotension
ECG changes
vtach, vfib
prolonged QT interval
*treat EKG changes with calcium gluconate..give calcium to lower threshold for cardiac arrhythmias
hypocalcemia assessment: mild to severe
chvostek’s sign
muscular contraction/twitching on the face
trousseau’s sign
arm curls in when BP cuff placed on
hypocalcemia: interventions
administer
Ca+2 supplements
PO: 1-1.5 hours after meals
IV: calcium gluconate
meds
vitamin D w/dietary Ca+2
phosphate binders: lower phosphate levels, increase Ca+2 due to inverse relationship
pain management
monitor
breathing
bone fx
chvostek and trousseau signs
labs
ECG
other
safety: seizure precautions, fall precuations, reorient if changes in LOC, lift/draw sheet
educate
decreased risk of osteoporosis: Ca+2, vitamin D, exercise (esp if weight bearing)
phosphate normal serum levels
serum phosphate: 3 - 4.5 mg/dL
phosphate functions
bone and teeth formation
essential to tissue oxygenation (RBCs)
cellular metabolism (ATP)
DNA and RNA synthesis
acid-base balance
Ca+2 regulation → inverse relationship
cell membrane structure
**influenced by PTH due to inverse relationship with Ca+2
phosphate is regulated by the kidneys → excreted by kidneys
phosphate dietary intake
most of the phosphate in our body comes from our diet
higher in phosphate
dairy products
meat and poultry
fish
lentils
split peas
chickpeas
almonds
sunflower seeds
whole wheat bread
brown rice
bran cereals
carbonated beverages (containing phosphoric acid)
lower in phosphate
fruits
vegetables
grains
starches
white bread
white rice
eggs
pasta
hyperphosphatemia serum level
serum level: > 4.5 mg/dL
hyperphosphatemia: patients at risk
increased intake
vitamin D intoxication
phosphate laxatives or enemas
production or release (cell damage)
hemolysis
rhabdomyolysis
tumor lysis syndrome
sickle cell, hemolytic anemia
hemolysis
reduced loss
renal insufficiency
hypoparathyroidism → less Ca+2 → more phosphate
thyrotoxicosis
hyperphosphatemia assessment
typically patients experience effects of hypocalcemia → bc inverse relationship w phosphate
neuro
tetany
faster nerve transmission
GI
abdominal cramping
diarrhea
nausea
CV
increased HR (prolonged QT interval)
other
decreased serum Ca+2
calcium deposits in skin, soft tissues, corneas, kidneys (longer-term consequence)
hyperphosphatemia interventions
prevention
identify and treat the cause (usually renal)
restrict phosphate-containing foods (stop diary)
IV fluids (to dilute) + diuretics to increase renal excretion
isotonic fluids → don’t wanna change serum osmolality → hydrate body and get rid of excess electrolytes
adminster phosphate-binding agents (sevelemer, Phos-Lo) → give with meals
bind to phosphate → less phosphate in the blood
hemodialysis may be necessary → if kidney’s aren’t functioning
hypophosphatemia serum level
serum phosphate < 3 mg/dL
hypophosphatemia: patients at risk
dietary
malnutrition
malabsorption of vitamin D
parenteral nutrition
chronic ETOH related to decreased dietary intake, diuresis
GI
vomiting
anorexia
chronic diarrhea
gastric suction
hormones
hyper-parathyroidism
more Ca+2 → loss phosphate
other
phosphate-binding antacids
diuretics
respiratory alkalosis
hypophosphatemia: assessment
symptoms usually only present when severe
symptoms are related to impaired cellular energy and O2 delivery
neuro
CNS dysfunction
confusion
coma
GU
renal wasting of Mg, Ca, and HCO3-
CV
arryhthmias
decreased stroke volume
MS
muscle fatigue → includes respiratory muscles
weakness
osteomalacia (softening of bones)
rhabdomyolysis
other
increased serum Ca+2
decreased tissue oxygenation
hypophosphatemia: interventions
identify underlying cause
phosphate supplementation
moderate - severe deficiency (<1 ng/dL) can be fatal
identify at-risk patients
oral or IV phosphate (no faster than 10 mEq/hr)
don’t give IV too quick → usually over 4 hours
monitor labs, vitals, ECG
magnesium normal serum level
serum magnesium: 1.3 - 2.1 mEq/dL
functions of magnesium
important cofactor in hundreds of enzyme systems
protein synthesis
blood glucose control
blood pressure regulation
strengthens bones and teeth
helps with transport of Ca+ and K+ across cell membrane
nerve impulses
muscle contractions
cardiac rhythm
magnesium: dietary intake
higher in Mg+2
dark chocolate
avocados
nuts
seeds
legumes
tofu
whole grains
fatty fish
bananas
leafy greens
lower in Mg+2
dairy products
spices/herbs
baby foods
fats/oils
poultry products
soups, sauces, gravies
sausages/luncheon meats
hypercalcemia serum level
serum magnesium: > 2.1 mEq/dL
hypermagnesia: patients at risk
excessive magnesium intake
laxatives/cathartics, antacids
IV magnesium (Tx of eclampsia) → used to treat seizures
metabolic disorders (shifts from ICF to ECF, impaired excretion)
kidney dysfunction
adrenal insufficiency
hypothyroidism
metastatic bone disease
tumor lysis syndrome
hypermagnesemia: assessment
magnesium is calming and depressing → worried abt their resp. system
CNS
headache
dizziness
drowsiness
confusion
respiratory depression
GI
nausea/vomiting
constipation
ileus
MSK
weakness
loss of DTRs
paralysis
GU
urinary retention
CV
vasodilation
facial flushing
hypotension
bradycardia
AV block
asystole
hypermagnesemia: interventions
hold Mg+2-containing products/food
calcium chloride/calcium gluconate IV for acute cardiac symptoms
gonna help protect and calm the heart
helps lower threshold for arrhythmias
move it out of the body
IV hydration + diuretics
monitor
VS
LOC
DTRs
hypomagnesemia serum level
serum magnesium <1.3 mEq/dL
hypomagnesemia: patients at risk
dietary
decreased diet intake
prolonged fasting/stavation
chronic ETOH → not absorbing magnesium
malabsorption syndromes → sometimes w gastric bypasses
GI fluid loss
vomiting
diarrhea
NG suctioning
other
pancreatitis
poorly controlled DM
PPI therapy → heartburn treatment
diuretics or other causes of excessive loss from urinary tract
hypomagnesemia: assessment
neuro
tremors
tetany
hyperreflexia
paresthesia
seizures
postitive babinski reflex
personality changes with agitation, depression, confusion, hallucinations
CV
ECG changes
arrythmias
TORSADES DE POINTES (deadly)
tornado in the heart
nonperfusable rhythm → shocking and decompressions don’t help
hypomagnesemia: interventions
replacement
mild
dietary changes: whole grains, nuts, legumes, magnesium salts, etc
severe
MgSO4 IM or slow IVPB → 1 mg/hr
monitor
LOC
Mg+ levels during replacement
VS
swallow/gag reflex
contents can go in lungs instead of stomach → aspiration pneumonia
common problem for elderly adults
can result in pneumonia and respiratory distress
DTRs
seizure precautions