Electrolytes Flashcards
Identify electrolyte imbalances
When you think Sodium (Na) think…
water - Sodium has many osmotic properties
What roles does Sodium play in the body?
-Intracellular metabolism, but it is the major extracellular cation
-Action Potentials - they are initiated when Na enters the cell
Hyponatremia etiologies
-Fluid excess
-sodium deficit
Hyponatremia s/sx
the swelling of these cells that are “dripping” in water is what causes a lot of the s/sx
Neuro > headache, fatigue, apathy, seizures, confusion, coma
Pulm > respiratory distress (pulmonary edema and vol overload)
CV > orthostatic hypotension, decreased CVP (b/c water is not staying inside the vessel)
GI > anorexia, nausea, vomiting, abdominal cramps, muscle weakness
Hyponatremia Tx
-slow replacement either PO or IV
recommended rate: < 8 mEq/L/day
What happens if we increase Na too quickly?
Osmotic Demyelination Syndrome - literally sucks water out of the myelin tissue surrounding the neurons
Hypernatremia etiologies
-fluid deficit
-sodium excess
Hypernatremia s/sx
-cells are super dry, no matter what the total body water is so, s/sx are r/t dehydration
Neuro > restlessness, irritability, lethargy, seizures, confusion, coma
Pulm > dyspnea
CV > tachycardia, orthostatic hypotension, dry mucous membranes, dehydration, flushed skin
GI/GU > decreased u/o (unless its DI)
Musculoskeletal > muscle weakness
Hypernatremia tx
-replace the volume that the pt has lost (there is an equation to figure how much water needs to be replaced)
-replacement must be done slowly (max speed of Na drop: 12 mEq/day)
-treat the underlying cause
What happens if we decrease Na too quickly?
Cerebral Edema - this will happen because water will move into the cells, causing swelling. This edema occurs b/c organic osmolytes that have accumulated during hypernatremia adaptation are slow to leave the cell during rehydration. Organic osmolytes are small solutes (e.g. amino acids, sugars, methylamines, and urea) that help cells maintain their volumes.
When you think of Potassium (K) think…
electricity
What roles does potassium play in the body?
-major intracellular cation
-maintains cellular osmolarity
-electrical neutrality and conductivity
-nerve impulses and cardiac contractility
-it is affected by pH (because cells are trying maintain their electrical balance, so K moves out of the cells and the H ions can take the K’s place inside the cells because they are of the same charge)
Hypokalemia etiologies
-decreased intake
-increased loss
-shift of K into the cells (alkalosis and hypothermia)
Will K be low or high in acidosis?
high
Will K be low or high in alkalosis?
Low
Hypokalemia s/sx
-these s/sx are r/t having lessened impulses
Neuro > lethargy, decreased reflexes, confusion, depression
CV > decreased BP, ST depression, QT prolongation, small or flattened T waves, U waves, dysrhythmias, cardiac arrest
GI > anorexia, n/v, distention, ileus
GU > dilute urine, water loss, thirst
MS > weak, flaccid, cramping, respiratory arrest
Hypokalemia tx
-replace it PO or IV - PO is absorbed better
-don’t give too quickly!
-double check your Mg level - adequate levels of Mg will help the body to absorb the K and hold onto it
Hyperkalemia etiologies
-excess intake
-decreased loss (renal failure)
-shift of K out of the cells (acidosis)
Hyperkalemia s/sx
-s/sx will be r/t cells being more excitable, “irritable” or “jumpy”
Neuro > numbness, paresthesia, hyporeflexia
CV > conduction disturbances, tall T waves, wide QRS, long PR, ST depression, idioventricular response, VF/asystole
GI > n/v/d
GU > oliguria, anuria
MS > early - irritability, cramping; late - weakness; flaccid paralysis (its like the cells run out of energy)
Hyperkalemia treatments
1 - protect cardiovascular function
2 - shift K into cells
3 - remove K
HyperK protect CV function tx
CaCl or Ca gluconate slow IVP - renders the myocardium less excitable by decreasing the effects of excess extracellular potassium
Ca Gluconate is preferred
HyperK shift K into cells tx
-IV insulin with a IV glucose chaser so BS doesn’t go too low
-Na Bicarb
-Albuterol - stimulates beta 2, beta 2 is also on the pancreas. So this stimulation tells the pancreas to release more insulin, but if the person has DM-II and pancreas doesn’t work/doesn’t release as much insulin anymore this really won’t work for them. This is used more in peds.
HyperK remove K tx
-loop diuretics - excrete it from the kidneys
-kayexalate - poop it out
-sorbitol - similar to kayexalate
-hemodialysis
Calcium roles in the body
-nerve impulses
-cardiac muscle contractility
-important role in action potential and pacemaker function
-needed to activate clotting cascades
-teeth and bones.. of course
-smooth muscle contraction and vasodynamics
Which organs regulate Calcium levels?
Intestines, bones and kidneys
Which endocrine gland monitors Ca levels?
Parathyroid gland
How does the parathyroid regulate Ca?
-If Ca is low, PTH is released and goes to the gut to pull Ca from the intestines. If there is no Ca there, PTH will pull Ca from the bones and at the same time PTH will go to kidneys and turns “off” the release valve for Ca.
-Calcitriol - hormone synthesized in the kidneys will promote reabsorption of Ca in the kidneys (you need healthy kidneys in order for to have calcitriol)
-Vitamin D is also needed to absorb Ca
-If Ca increases to normal levels, the thyroid will release Calcitonin which goes to the bones and kidneys, tell them to stop releasing Ca into the blood
Will Ca be low or high in alkalosis?
Low
Will Ca be low or high in acidosis?
high
What is the relationship between Ca and Phos?
inverse
they are enemies
What is the relationship between Ca and Mg?
correlating
they are friends
Hypocalcemia etiologies
-Excess loss
-inadequate intake
-decreased iCa - (e.g. blood transfusions where the citrate binds to all the free Ca, making it useless)
-GI/bone absorption
-alkalosis
Hypocalcemia s/sx
-s/sx are r/t nerve irritability
-neuro > tingling, seizures, hyperreflexia
-CV > dysrhythmias, prolonged QT, cardiac arrest, bruising, bleeding
-Pulm > laryngospasm, bronchospasm
-GI > increased peristalsis, n/v/d
-MS > osteoporosis, fractures, abnormal deposits of Ca in body tissues, muscle spasm, tetany
2 signs of hypocalcemia (named after people who found them)
Chvostek’s sign - tapping the pt’s forehead/temple region, activating CN VII, face will twitch
Trousseau’s sign - tourniquet or BP cuff to upper arm, ulnar nerve becomes ischemic and their hand twitches
hypocalcemia tx.
-Replace PO or IV
-Double-check if Mg also needs to be replaced - increasing Mg will allow the body to hold onto the Ca you’re giving it
-If phos is too high, Ca won’t be able to stick around - may need a phosphorus binder
Hypercalcemia etiologies
-excess intake
-loss from bones
-prolonged immobility causes increased mobilization of Ca from your bones
-acidosis
Hypercalcemia s/sx
-these s/sx are r/t nerve “depression”/lethargy/sluggish (its like too much of a good thing)
-Neuro > decreased reflexes, lethargy, coma, seizures
-CV > depressed activity, dysrhythmias, shortened QT, cardiac arrest
-GI > decreased motility of GI tract, increased peristalsis, n/v, constipation
-GU> kidney stones, flank pain
-MS > muscle fatigue, hypotonia, bone pain, osteoporosis, fractures
Hypercalcemia tx
-volume expansion: dilute
-loop diuretics: pee it out
-corticosteroids: block Ca absorption in GI tract
-calcitonin or mithramycin: stops kidneys and bones from releasing Ca into the blood
-treat the underlying cause
When you think of Mg think of…..
Energy
What are the roles of Mg in the body?
-essential for production of energy
-Na-K ATPase pump
-cell membrane stabilization
-vasodilating effects
-influences neurotransmitter release
Hypomagnesemia etiologies
-Excess loss
-inadequate intake
-impaired absorption
-alkalosis
Hypomagnesemia s/sx
-think about lots of squeeze, excitability
-Neuro > agitation, depression, confusion, convulsions, paresthesia’s, ataxia, hyperreflexia, vertigo, seizures
-DV > dysrhythmias, torsades, tachycardia, HTN, increased SVR
-GI > n/v
-MS > cramps, spasticity, tetany
hypomagnesemia tx
-replace it!
What happens if we replace Mg too quickly?
Mg has vasodilatory effects; therefore, we could see flushing of the skin, hypotension, and bradycardia.
Hypermagnesemia etiologies
-increased intake
-renal insufficiency
-acidosis
hypermagnesemia s/sx
-these s/sx r/t low energy
-Neuro > hyporeflexia, lethargy, coma
-CV > dysrhythmias, hypotension, flushed/warm skin
-Pulm > respiratory depression, apnea
-MS > muscle fatigue, hypotonia, bone pain, osteoporosis, fractures
hypermagnesemia tx
-vol expansion: to dilute
-loop diuretics: to excrete it
-decrease intake (e.g. is the pt taking any laxative or antacids containing Mg?)
-IV insulin and IV glucose ‘trick’ (we can do this because Mg follows K)
-treat acidosis
-Hemodialysis or continuous ambulatory peritoneal dialysis
