A better deck of flash card on electrolytes
what is the most abundant intracellular cation?
Potassium
what are functions of potassium
allows transmission of electrical impulses, helps impulses flow smoothly, w/o potassium things slow down. too much and muscle get hyperactive
what systems does potassium directly affect
the heart, GI tract, MS system.
Acid base balance - trades places with hydrogen ions to balance charges
0.1 decrease in in pH - a 0.5 increase in K
hypokalemia
think low and slow! less than 3.5.
the heart has flattened T waves and prominant U, waves. orthostatic hypotension, weak thready pulse, dysarythmias,
muscular cramping, flaccid paralysis, hyporeflexia, muscle weakness.
neuro changes - include altered mental status, letharfy, decreased LOC
Gi symptoms - hypoactive bowel sounds, constipation, andominal distention, paralytic ileus, can lead to small bowel obstructions
therapeutic management of hypokalemia
prevent more loss with IV K or PO K - REPLACE SLOWLY
switch diuretics - no loops diuretics or thiazides
eat k rich foods such as banans, kale, melons
cardiac monitor
assess respiratory function, can cause respiratory depression.
hyperkalemia
> 5 think fast!
CV = bradycardia, hypotension
EKG = tall peaked T-waves, prolonged PR intervals, Wide QRS, heart block, asystole, Vfib,
MS = twitching, numbness, weakness
GI - hyperactive bowel sounds, spastic colon, diarrhea.
therapeutic management of hyperkalemia
potassium decreasing meds = kayexelate
K-wasting diuretics, insulin and D50, albuterol, bicarb, calcium gluconate.
cardiac monitoring
k restricted diet
salt substitues should have potassium in them
dailysis
sodium!
the most abundant ECF cation
it controls fluid distribution between the ICF and ECF
normal levels is 135meq/l - 145meq/l
sodium is a real muscle mommy
she is everyone’s best friend.
she controls fluids between the ECF and ICF
inside our vessel we have solvent, and we have sodium. sodium is the solute. sodium will always try to perfectly dissolve solute and solvent while being balanced. thats where osmolarity of blood comes from
if there is a bunch of fluid outside the cell, sodium leaves the cell to help the balance. if theres a lot of solute concentration in the cell then sodium will bust her ass in to the cell to balance that out.
main functions of sodium
most abundant ECF cation
balances osmolarity
muscle contraction
nerve impulses
hyponatremia causes
(actual loss of Na)
<135meq/l
sweating
wound drainage
low Na diet
diuretics ( thiazide and loop)
hypoaldosternism
hyponatremia causes
(increase in fluids like h2o)
SIADH
water intoxication
freshwater submersion
insatiable thirst
hypotonic fluids
hypernatremia
(actual increase in Na)
steroids
oral ingestion
table salt
hypertonic saline (1.5%, 3%, 5%)
cushings syndrome
hypernatremia
(relative fluid loss)
NPO
fever
hyperventilation
dehydration
infection
assessment of hyponatremia
N - behavior changes , increased intracranial pressure, cerebral edema, seizures
ms - weaknes (resp muscles) deacreased DTRs
GI - motility, NVD, stomach cramps,
CV - hypovolemia - weak pulse, tachycardia, hypotension, dizziness,
hypervolemia - bounding pulses, high bp.
hypernetremia
N - cellular dehydration in brain cells
hypovolemic - irritable, confused, manic, cranky
hypervolemic - lethargic, drowsy, stupor, coma,
MS - muscle twitching cramps, weakness,
CV - heart contraction deacreases
hypovolemic - deacreased BP, weak pulses
hypervolemic - increased BP, JVD, bounding pulses
extreme thirst
dry mucous membranes
dry/hot skin
therapeutic management with hyponatremia
replace fluid slowly
prevent pontine myelionolysis
neuro damage by over correction
locked in syndrome
increase sodium level by 0.5meq/hr - go slow
drugs:
stop Na wasting diuretics
IV 0.9% NaCl if hypovolemic
hypertonic saline 3%
osmotic diuretics
lose h20 not Na
increase sodium intake
free water restriction
therapeutic management of hypernatremia
often caused by steroids
bring levels down slowly
hypotonic fluids - 1/2 NS, D5W
if hypervolemic give Na wasting diuretics
get dietician in there
Na restriction
increase free water.
calcium !
8.6 - 10.4 mg/dl cation
main functions:
stored mostly in bones
mineralizes bones and keeps them hard
helps nerve impulses and in muscle contraction
activates actin and myosin
neuromuscular processes
coagulation
controlled by pth and thyroid hormone and vitamin D
inverse relationship with phosphorous - when calcium is low phosphorous is high
causes of hypocalcemia
<8.6mg/dl
renal failure
malnutrition/malabsorption
alcoholism
defficiency in albumin, Mg, or vitamin D
vitamin D is required for absorption of calcium in the gut
hypoparathyroidism
hyperphosphatemia
causes of hypercalcemia
hyperparathyroidism
malgnancy
vitamin D toxicity
excessive nutritional intake
assessment of hypocalcemia
neuromuscular - sputtering and irritable
parasthesias - tetany, spasm
chvosteks sign - cheek twitching when stroked \
trousseaus sign - inflate BP cuff - hand and wrist spasm
cv - insufficient contractility, HR decreased, decreased BP, weak pulse
EKG - prolonged st, and qt interval, that means the time it takes the signal to get from the sa node to the AV node and down the ventricles is delayed.
GI - increased bowel sounds, cramping, diarrhea.
skeletal - osteoporosis
assessment of hypercalcemia
neuromuscular - exhausting muscles because it overly excites the muscles that they give out
weakness,
decreased DTRs
decreased LOC
CV - decreased HR, peripheral cyanosis, DVT pr clotting
EKG - shortened QT wave
GI - decreased peristalsis, leads to constipation, decreased bowel sounds, abdominal pain, the gut is worn out
therapeutic management of hypocalcemia
replace Ca with IV or PO
give with vitamin D or aluminum hydroxide to increase absorption
muscle relaxants
decrease stimuli
increase nutrition intake - broccoli, coconut, milk or any dairy products
therapeutic management of hypercalcemia
goal is to decrease calcium levels, rehydrate, the kidneys should excrete excess calcium
IV fluids 0.9% NS
drugs such as calcium binders, calcium reabsorption inhibitors
phosphorous
calcitonin
biphosphonates
NSAIDS
dialysis
cardiac monitoring
chloride cl-!
96-108meq/l
main functions:
most abundant extracellular anion
sodium and chloride are married
works with sodium to maintain fluid balance
binds with H-HCL - to stomach acid
inversely related to hco3 (bicarb) when one goes up the other goes down
directly related to Na + K so when on goes up so does the other one
hypochloremia
> 108meq/l
volume overload
CHF
water intoxication
metabolic alkalosis - HCO3 goes up, so Cl goes down
actual “salt” losses:
burns
sweating
cystic fibrosis
addisons disease
with CHF patients or water intoxication we see a low cl
patients lose salt through skin and cystic fibrosis, and addisons disease
hyperchloremia
<96 meq/l
dehydration
metabolic acidosis-bicarb is low
acute renal failure
cushings syndrome
assessment hypochloremia
rarely produces obvious symptoms
presents s/s of hyponatremia
fluid shifting out of th vessels and into th cells and tissues
behavior changes
increased ICP
cerebral edema
muscle weakness
hyperactivity in the GI tract
assessment hyperchloremia
cellular dehydration
behavior changes
dry mouth, thirst, hot dry skin,
muscle twitching and issues with cardiac contractility
presents with s/s of hypernatremia
therapeutic management of hypochloremia
goal - correct imbalance,
treat underlying cause
give 0.9% sodium chloride
check out other electrolytes like sodium and bicarb
could give salt orally but would take too long
therapeutic management of hyperchloremia
goal - correct imbalance
treat underlying cause
give bicarb
avoid Na pr NaCl intake
give lactated ringers for IV fluids
wont be abnormal by itself
magnesium!
normal range - 1.6-2.6mg/dl
main functions:
60% stored in bones and cartilage
skeletal muscle contraction
carbohydrate metabolism
ATP formation
activation of vitamins
cellular growth
direct relationship with Ca++ so if one goes up then vice versa
hypomagnesemia causes
ETOH abuse
renal failure
malnutrition/malabsorption
hypoparathyroidism
hypocalcemia
diarrhea - Mg is lost in stool
hypermagnesemia causes
excess intake of Mg - containing meds
overcorrection with Mg supplementation (IV or PO)
renal failure
fairly uncommon
hypomagnesemia assessment
neuromuscular - numbness and tingling, tetany, seizures, increased DTRs
CNS - psychosis, confusion
GI - decreased motility, constipation, anorexia
EKG - prolonged QT
hypermagnesemia assessment
Cv - severe bradycardia, cardiac arrest, vasodilation, hypotension
EKG - prolonged PR, wide QRS
CNS - drowsy, lethargic, coma
neuromuscular - slow/weak muscle contraction, decreased DTR
therapeutic management hypomagnesemia
replace mg
PO - magnesium hydroxide
not magnesium citrate
IV - 1g per hour (SLOW)
treat the cause:
diuretics and aminoglycosides, phosphorous
monitor EKG and DTRs
therapeutic management of hypermagnesemia
treat the cause:
MG containing drugs (OTC antacids) or iv fluids
loop diuretics
give calcium gluconate to protect heart
dialysis
always give magnesium before potassium. Why?
if potassium is given first, the potassium will not absorbed in the presence of magnesium.
phosphorous!
normal range - 3 -4.5
cellular metabolism and energy production
ATP production (adenosine triphosphate)
forms phospholipid bilayer of cell membranes - not nough phos, not a good cell membrane
bones and teeth
inverse relationship with Ca++ ( if phos goes up calcium goes down
causes hypophosphatemia
malnutrition/starvation
TPN
Refeeding syndrome
the body responds excessively to the extra nutrition and starts shifting fluids around.
causes hyperphosphatemia
renal failure
tumor lysis syndrome
excessive intake
hypoparathyroidism
hypocalcemia
assessment hypophosphatemia
symptoms related to a lack of energy ATP and damage to cell membranes
CV - cardiac output and stroke volume and weak pulses
MS - weakness, possible rhabdomyolysis (due to cell damage)
skeletal - decreased bone density, fractures
CNS - irritable -, seizure, coma
therepeutic hyperphosphatemia
replace phos
IV must be given slowly
drugs that reduce phosphate:
antacids, calciu, osmotic diuretics, phosphate bonders, phos-lo
phos rich foods
fish chicken beef
ca rich foods such as dairy, greens
assessment hyperphosphatemia
typically tolerated well - doesn’t produce symptoms
often associated with hypocalcemia
hyperphosphatemia therapeutic management
phosphate binders
give with meals - the whole point is to bind phosphorous with meals so it doesnt get absorbed
manage hypocalcemia
major intracellular electrolytes
potassium + magnesium
major extracellular electrolytes
sodium and chloride
cations
sodium
potassium
calcium
magnesium
hydrogen
anions
bicarbonate
phosphate
chloride
sulfate
fluids and electrolytes are regulated by what systems:
endocrine, cardiovascular, kidneys, gastrointestinal
