potassium Flashcards
Potassium is a major____cation
ICF cation- most of the potassium
Potassium serum range is_____.
98% ICF
narrow; little change in potassium has a huge impact because the range is narrow;
small changes can be significant cardiac response)
Potassium is excreted by
kidneys
if potassium concentration within muscle cells is about 140mEq/L; ECF is 3.5-5.0mEq/L then…
sodium potassium pump in cell membrane maintains this concentration difference by pumping potassium into the cell and sodium out.
B/c ratio of ECF Potassium to ICF potassium is the major factor in the resting membrane potential of nerve and muscle cells, neuromuscular and cardiac functions are commonly affected by potassium imbalances
disruption in dynamic equilibrium between ICF and ECF potassium can cause clinical problems.
potassium regulates intracellular osmolality and promotes cellular growth.
potassium is required for glycogen to be deposited in muscle and liver cells
diet and meds is source of potassium
fruits, dried fruits, veggies
IV fluids, transfusion of stored hemolyzed blood, meds
how does the body regulate potassium
kidneys-primary route for potassium loss (90%)
rest is loss in sweat and stool
inverse relationship between sodium and potassium
factors that cause sodium retention (low blood volume, inc aldosterone levels) cause potassium loss in urine
large urine volume= excess loss of potassium in the urine ( a lot of urine= a lot of potassium loss in urine)
what happens if there is an impaired kidney function?
retained potassium= toxic levels
potassium labs
3.5-5.0 mEq/L
hyperkalemia- pts at risk
(high serum potassium) impaired renal excretion shift of K from ICF to ECF massive intake of K dec renal excretion (RF most common cause of hyperkalemia) hypoaldosteronism K containing salt substitute K shifting from cells to plasma impair entry of potassium into cell (digoxin- higher ECF K concentration)
what is the most common cause of hyperkalemia?
RF
hyperkalemia- pts at risk: what is hypoaldosteronism?
addison’s disease: adrenal gland insufficiency
adrenal insufficiency with aldosterone deficiency leads to retention of K
hyperkalemia- pts at risk: what happens when K shifts from cells to plasma?
k sparing/conserving diuretics;
cell destruction- excessive exercise, catabolism(every time a cell dies, its going to release K)
factors causing K to move from ICF to ECF
hyperkalemia- pts at risk: factors causing K to move from ICF to ECF
metabolic acidosis-( exchange of hydrogen ions moving into the cell)
massive cell destruction (burn, tumor, lysis, severe infection)
exercise
hyperkalemia- pts at risk: development of hyperkalemia
K-sparing drugs and aldosterone receptor blockers and angiostensin-converting enzyme (ACE) inhibitors
reduces kidney’s ability to excrete potassium
hyperkalemia- pts at risk: inc cell excitability( inc concentration of K outside the cell)
as K levels inc, pt experiences cramping leg pain and weakness/paralysis of skeletal muscle
hyperkalemia- pts at risk: inc cell excitability( inc concentration of K outside the cell)- cardiac/ meds
most clinically significant for hyperkalemia
altered cardiac function (ask about meds; K sparing meds, ACE inhibitors); dysrhythmias
hyperkalemia- pts at risk: inc cell excitability( inc concentration of K outside the cell) - NM
early: muscle twitching, paresthesia in hands, feet and around mouth
later: skeletal muscle weakness (muscle groups)
respiratory muscles affected with very high K levels
hyperkalemia- pts at risk: inc cell excitability( inc concentration of K outside the cell) - GI
smooth muscle- hyperactivity
abdominal cramping and diarrhea
Hypokalemia- pts at risk
low serum K
inc loss of K from an inc shift of K from ECF to ICF
Hypokalemia- pts at risk: GI Loss
most common causes- GI and kidneys
diarrhea, laxative abuse, vomiting, and ileostomy drainage
hyperaldosteronism- adrenal tumor
Hypokalemia- pts at risk: Renal Loss
low magnesium level or is diuresing
(esp in pt with elevated aldosterone levels)
aldosterone is released when circulating blood volume is low (causing Na retention in kidneys with a loss of K in urine)
low magnesium stimulates renin release and inc aldosterone levels -> results in K excretion
Hypokalemia- pts at risk: Meds
K wasting diuretics (Furosemide- lasix; Hydrochlorothiazide- HCTZ) corticosteroids laxative overuse steroids excessive insulin- cell uptake of K
Hypokalemia- pts at risk: Alkalosis
shift of K into cells in exchange for hydrogen
this lowers K in ECF which causes hypokalemia
Hypokalemia- Assessment
alters resting membrane potential
results in hyperpolarization and impaired muscle contraction (involves cardiac and muscle functions)
Hypokalemia- Assessment: cardiac
most serous clinical problem
dysrhythmias- EKG changes( dec BP- orthostatic hypotension); weak thready pulse; inc digoxin toxicity (inc sensitivity of excitable membranes with hypokalemia; always assess latest K levels before administering digoxin; do not administer with low K)
Hypokalemia- Assessment: Musculoskeletal
a stronger stimulus is needed;
dec excitability of cells;
skeletal muscle weakness, fatigue (dec hand grasp, Dec DTR, leg cramps), respiratory muscle weakness(priority assessment)
Hypokalemia- Assessment: GI (alteration of smooth muscle function)
dec peristalsis: dec bowel sounds- (abdominal distention; N/V; cramping; constipation); paralytic ileus with severe hypokalemia
Hypokalemia- Assessment: Respiratory
priority assessment with hypokalemia: breath sounds; ease of respiratory effort; rate and depth; color of nail beds/mucous membrane
weak muscle
shallow respiration
Hypokalemia- Assessment: nonmucsle function
by impairing insulin secretion: causes hyperglycemia
Hyperkalemia- Nsg Dx: risk
activity intolerance- related to lower extremities muscle weakness(fatigue)
electrolyte imbalance- excessive retention or cellular release of K (diarrhea- inc peristalsis)
injury related to lower extremities muscle weakness and seizures (falls)
Hypokalemia- Nsg Dx: risk
activity intolerance- lower extremity muscle weakness
electrolyte imbalance- excessive loss of K
injury related to muscle weakness and hyporeflexia
constipation
dc CO
Hyperkalemia- Nsg DX: complicaitons
dysrhythmias, CO
Hypokalemia- Nsg Dx: complications
dysrhythmia
Hyperkalemia- Goals
dec K and treat cause
Hyperkalemia- Goals: treatment
eliminate oral and parenteral K intake
inc elimination of K (using diuretics, dialysis, and ion exchange resins; insulin with glucose)
force potassium from ECF to ICF (using IV administration of regular insulin; IV sodium bicarbonate for correction of acidosis)
reverse membrane potential effects of elevated ECF K by administering IV calcium gluconate ( calcium can immediately reverse the membrane excitability)
Hyperkalemia- Goals: treatment of mild potassium evaluation
withhold K from diet and IV sources
inc renal K elimination by administering fluids and loops or thiazide diuretics
Hyperkalemia- Goals: treatment of moderate
additionally receive one of the treatment to force K into cells; usually IV insulin and glucose
Hyperkalemia- Goals: monitor EKGs in clinically significant hyperkalemia
to detect dysrhythmias
dangerous cardiac dysrhythmias should receive IV calcium gluconate immediately
Hyperkalemia- Goals: Monitor BP
B/c rapid administration of Ca can cause hypotension
Hyperkalemia- Goals: hemodialysis
effective means of removing potassium from the body in the pt with RF
Hyperkalemia- Goals: monitor
telemetry K lab report bowel sound and stool UOP muscle tone and all body systems affected
Hypokalemia- Goals: treatment
oral or IV KCl supplements and dietary intake of K
EXCEPT: in severe deficiencies; KCl is not given unless there is a urine output of at least 0.5mL/kg of body weight per hour
Hypokalemia- Goals: inc K intake
foods(bananas, cantaloupe)
PO supplements: can be gastric irritants
(K-dur, micro-K, slow-K: dont crush/chew; dont open capsule)
intravenous K: monitor UOP; use large vein sites as K b/c is irritating
Hypokalemia- Goals: diuretics
use K sparingly (spironoalctone)
hold loop and thiazide diuretics( this inc K excretion)
Hypokalemia- Goals: treat constipation
colace
miralax
metamucil
surfak
Hypokalemia- Goals: safety measures
skeletal muscle weakness (remove throw rugs, assist with ambulation)
Hypokalemia- Goals: monitor
telemetry
VS, HR, Respiratory status( critically ill pts should have cardiac monitoring to detect cardiac changes due to K imbalance)
serum K levels and UOP (pts on digoxin therapy have an inc risk of toxicity if serum K level is low)
