Potassium Disorder Flashcards
What are the physiological functions of potassium
Cell metabolism, glycogen and protien synthesis, electrical action potential
What is the distribution of total body K+, how much intracellular, how is it distributed intracellularly, extracellular
50 mEq/kg, 98% (150 mEq/L), 75% skeletal muscle/25% liver and blood cells, 2% (4mEq/L) extracellular
What are mechanisms that cause hypokalemia
Stimulation of NA/K ATPase pump, intracellular shift of K+, metabolic alkalosis
What are mechanisms that cause hyperkalemia
inhibition of Na/K ATPase pump, release of K+ from cells, metabolic acidosis
What are conditions that would cause stimulation of Na/K ATPase pump (drive K+ in)
Excess insulin, Beta 2 adrenergic agonist, alpha 1 antagonist, aldosterone
What are conditions that would inhibit Na/K ATPase pump (slow K+ in)
Lack of insulin, Beta 2 adrenergic antagonist, alpha 1 agonist, digoxin toxicity
What are conditions that would cause a release of K+ from cells
injury/trauma, exercise, catabolism, hyperosmolarity
T/F: Anabolism causes an intracellular shift of potassium
True
What are determing factors for the degree of how much potassium leaves the body
a very high potassium concentration, presence of aldosterone, delivery of sodium water into the kidney
Why does metabolic acidosis cause hyperkalemia
In order to compensate for high H+ the hydrogen ions are pushed in and K+ is pushed out in order to keep the electrostatic balance
Why does metabolic alkalosis cause hypokalemia
In order to compensate for low H+ the hydrogen ions are pushed out and K+ is pushed in in order to keep the electrostatic balance
What is the inverse relationship between ph and K+
every increase in ph of .1 leads to a decrease of 0.6 mEq/L
What is the normal range for K+
3.5-4 mEq/L
What range is considered hypokalemia
less than 3.5 mEq/L
Which patients are more likely to suffer complications from hypokalemia
congestive heart failure, left ventricualr hypertrophy, cardiac ischemia
What are outcomes of uncorrected hypokalemia
Essential hypertension, ischemic and hemorrhagic stroke, arrhythmias, death
What are the causes of hypoalkemia
insufficient dietary intake, metabolic alkalosis, periodic paralysis, hyperaldosteronism, diuretics/osmotic diuersis,hypomagnesia
What are medications that may cause intracellular shift of K+ causing hypokalemia
Beta 2 adrenergic agonists (albuterol), phosphodiesterace inhibitors (theophylline, caffeine), insulin, barium or verapamil overdose
How do diuretics cause hypoalkemia
Na+ reabsorption is hindered causing a large amount to be in the kidney, the body will then activate the Na/K ATPase in the collecting duct causing K+ to be secreted out into the urine
What are the signs of hypoalkemia
muscle weaknes (more lower than upper), constipation. EKG changes, arrhythmias, ascending paralysis
In EKG readings what wave changes due to hypokalemia and how is it changed
T wave, inversion
How does hypoalkemia increase the risk for hypertension
low release of sodium in the urine, low direct vasodilation, high sensitivity to norepinephrine or angiotensin 2
How does hypoalkemia increase the risk for stroke
higher blood pressure, higher free O2 free radicals and higher arterial thrombosis
T/F: An increase in K+ intake can cause a lower stroke rate in pateints and decrease blood pressure
True
What is the goal range for patients who have hypokalemia
greater than or equal to 4 mEq/L
What are the primary ways to treat hypoalkemia
treat the underlying cause, treat hypomagnesia, avoid drugs that drop K+
Around what range should the patient have a moderate to sever symptoms of hypoalkemia
3.0- 2.7 mEq/L, less than 2.7 mEq/L
In patients who have hypokalemia what is the method to estimate the potassium defecit
If the K+ is greater than or equal to 3.0 mEq/L; each 0.1 mEq/L lower in the K+ level represents a 10 mEq deficit, If the K+ is less than 3.0 mEq/L, each 0.1 mEq/L represents a 20 mEq deficit
Which food has the highest potassium content
dried figs molasses, nuts avocados ban cereals lima beans
T/F: Dietary changes cause an immediate change in K+
False: these changes happen over days
What is the oral potassium supplement dosing that aides in hypokalemia
divide the dose into no more than 40mEq doses at a time every 3-4 hours to avoid Gi ADR
What potassium oral supplement is used most often for hypoalkemia, What is the dosage strength,why
KCl controlled release, 10 mEq, less likely to cause GI irritation
What are the parenteral main routes for Potassium supplements
IVPB or continuous infusion, must be at a rate and mixed
T/F: Potassium can be administered IM, IVP or SC
False: Potassium can NEVER be administered IM, IVP, or SC
What is the rate of administration for potassium supplementation through peripheral access or non cardiac monitoring, maximum concentration for continuous flowing IV fluids and IV piggyback
10 mEq/hr, 40-60mEq/1000ml and 40meq/250 ml
What is the rate of administration for potassium supplementation through central access with cardiac monitoring, what is the maximum concentration
20 mEq/hr but up to 40-100 mEq/hr in rare life threatening cases 40mEq/100ml
What is the range that diagnosis as hyeralkemia, what is susceptible population of patients
greater than 5 mEq/L, acute and chronic renal disease
Causes of pseduo-hyperalkemia
hemolysis, thrombocytosis, leukocytosis, erythrocytosis
What are the causes of hyperkalemia
dietary source, medications (penicillin), extracellular shift of K+
T/F: Hyperosmolarity from hyperglycemia can cause hyperkalemia
True
Which medications cause impaired K+ excretion leading to hyperkalemia
spironolactone, eplerenone, trimethoprim, NSAIDS, tacrolimus cyclosporine, amiloride
What are symptoms of cardiac hyperkalemia
slower ventricular conduction, decreased duration of action potential, depolarizes the cell membrane, EKG changes, arrhythmia (AV block,cardiac arrest)
In EKG readings what wave changes due to hyperkalemia and how is it changed
T- wave, Tall peaked
What are the primary treatments for hyperkalemia
treat the underlying cause, asses for pseudohyperkalemia
In severe hyperkalemia what are the objectives to reach for a patient
membrane stabilization (restore the normal gradient with the resting membrane potential), intracellular shifting ( stimulate Na/K ATPase, increase serum pH), elimination (increase delivery of Na+ and urine flow rate)
What drug will stabilize the membrane, what is checked after treatment
Calcium IV for 30-60 mins, EKG
What are the neuromuscular symptoms of hyperkalemia
muscle twitching, cramping, flaccid paralysis, paraesthesias
What is the prophylactic dose for potassium if diuretics are needed
10-20 mEq per day and titrate as needed
Around what range should a patient have moderate to severe hyperkalemia symptoms
6.5-8, greater than 8
What drug will be used to stabilize the intracellular shift of hyperkalemia, what is the dose, what is a risk
insulin 10 units IV +/- 50 ml of D5W, hypoglycemia
In order to treat hyperkalemia when is insulin given with D5W
When the patients glucose is less than 200
T/F: Insulin given for hyperkalemia should be taken from 1 to 2 hours
False: Insulin should be IV for 4-6 hours
What drug will be used for hyperkalemia caused by metabolic acidosis
NaHCO3
What are the 3 medications/methods used for elimination in hyperkalemia
sodium polystyrene sulfonate, furosemide, dialysis
What are the two distribution routes for sodium polystyrene sulfonate, what are the doses for each
PO: 15-30 grams in 70% sorbitol every 4-6 hours, Rectal: 30-60 grams per rectum every 4 to 6 hours
T/F: Sodium polystyrene must be eliminated from the body no matter what the route is
True