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-Exam 1, Dr. Wai
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3.5-5
ECF potassium concentration goal range ___ mEq/L
potassium
most prevalent ICF cation
ICF concentration 140 mEq/L
ECF concentrations are not reflective of total body stores
regulates many biochemical processes in the body
required cell metabolism, protein, and glycogen synthesis
key cation for electrical action potentials across cellular membrane -cardiac conduction
potassium homeostasis
K concentrations are determined by the relationship between the following:
K intake
GI absorption and urinary excretion → malabsorption/chron’s, kidney disease
hormones
acid base balance
body fluid tonicity
insulin
increase cellular K uptake by stimulating cell membrane Na/K/ATPase
catecholamines
increase cellular K uptake by stimulating cell memnbrane Na/K/ATPase
aldosterone
promotes K+ excretion in collecting duct
angiotensin II
stimulates aldosterone secretion
relationship between serum and total body potassium
changes in serum K+ are directly proportional to changes in total body potassium (TBK)
relationship is not linear
helpful to determine magnitude of clinical problems
serum K levels drop approximately 0.3 mEq/L for every 100 mEq reduction in total body potassium
distributed ICF »»»» ECF
insulin, catecholamines, aldosterone, angiotensin II
which hormones DECREASE serum potassium concentrations?
hypokalemia
plasma K+ concentration < 3.5 mEq/L
common clinical problem → 21% of hospitalized patients
easily reversible → may be life threatening if severe
midl to moderate → increased morbidity and mortality in patients with cardiovascular disease
major causes of hypokalemia
decreased K+ intake
eating disorders
total parenteral nutrition
starvation
increased GI losses
vomiting
diarrhea
tube drainage (nasogatric tube output)
laxative abuse
increased entry into cells
elevated ECF pH (alkalosis)
increase availability of insulin *****
elevated B adrenergic activity
hypokalemic periodic paralysis
etc
increased urinary losses
diuretics (loop)
amphotericin B
others
increased sweat losses
dialysis
plasmapheresis
diuretics (loop)
major cause of renal losses with hypokalemia
increased availability of insulin
main cause of hypokalemia due to increased entry into cells
drug induced hypokalemia
loop and thiazide diuretics most common
transcellular potassium shift
increased renal potassium loss/excretion
increased GI loss
transcellular potassium shift
catecholamine B2-adrenergic agonist (epinephrine, norepinephrine)
decongestants
bronchodilators (albuterol)
theophylline and caffeine
verapamil intoxication
insulin (high dose) ****
chloroquinolone intoxication
increased renal potassium loss/excretion
diuretics (loop, acetazolamide, thiazides)
mineralocorticoids
antibiotics (penicillins, high doses)
drugs associated with Mg depletion
increased GI loss
sodium polysystrene sulfonate
hypomagnesemia
seen concomitantly in 40% of patients
other cause of hypokalemia
low mg decreases intracellular K+
impairs the function of Na/K/ATPase
promotes renal K wasting
hypokalemia clinical manifestations
majority of healthy patients with mild hypokalemia are asymptomatic
symptoms related to the degree and rate of development
mild to moderate symptoms: cramping, weakness, malaise, myalgia
symptom manifestation: cardiovascular, muscular activity
hypokalemia cardiac manifestations
arrhythmias
ECG changes
arrhthymias
increased risk in elderly patients or patients with underlying heart disease
can include:
bradycardia, heart block
atrial flutter, paroxysmal atrial tachycardia
ventricular fibrillation
increased digoxin toxicity
ECG changes
ST- segment depression or flattening
T wave inversion
U wave elevation
hypokalemia neuromuscular manifestations
results from hyperpolarization of skeletal muscle
may include:
muscle weakness
cramping
easy fatigability
myalgias
hypokalemia general recommendations
maintenance: potassium dosage of 20 mEq/day is usually sufficient to prevent hypokalemia from occuring
treatment: doses of 40-1000 mEq are usually sufficient to treat hypokalemia
approximately 10 mEq KCl will raise serum by 0.1 mEq/L (when serum K < 3, will require more
0.1
approximately 10 mEq KCl will raise serum by __ mEq/L (when serum K < 3, will require more
mild to moderate hypokalemia (3-3.4 mEq/l) treatment
oral administration of 10-20 mEq of potassium given 2-4 times per day
severe hypokalemia (<3 mEq/L) or symptomatic hypokalemia treatment
IV or PO administration of 40 mEq, 3-4 times per day
monitor serum K levels every 4 hours
monitor ECG changes
potassium salts
hypokalemia treatment
available in different salts: chloride, phosphate, bicarbonate
potassium chloride supplement
preferred agent for hypokalemia
most effective for common causes
diuretic and diarrhea induced loss of K+ and chloirde
potassium phosphate supplements
hypokalemia treatment
reserved for patients with loss of both K and phosphate
potassium bicarbonate supplements
hypokalemia treatment
for patients with hypokalemia and a metabolic acidosis
IV potassium
hypokalemia treatment
more dangerous than PO
burning sensation, risk of extravasation
limit use to: severe cases of hypokalemia (<2.5), symptomatic patients (ECG chages, muscle spasms, patients unable to tolerate PO)
should be mixed in saline containing solutions (0.9 or 0.45% NaCl)
SLOW infusions
IV potassium limits
severe cases of hypokalemia (<2 mEq/L)
symptomatic patients: ECG patients, muscle spasms, patients unable to tolerate PO
IV potassium dose
hypokalemia treatment
20-60mEq IVPB or added to fluid bag
most patients receive 10 mEq/hr
monitor serum K levels every 2-4 hrs
2-4
when giving IV potassium monitor serum K levels every ____ hours
magnesium
always replace low __ in patients first
hypokalemia alternative therapy
diet- spinach, figs, seaweed, beets, carrots, cauliflower, bananas, beef, pork, nuts, avocados, dried fruits
potassium sparing diuretics- commonly given with potassium wasting diuretics, amiloride, triamtere, spironolactone
insulin, furosemide, vomiting
67 you M with CHF and DM 2 presents to ED with N/V, muscle cramps.
Home meds: Lantus 30 mg SQ QHS, lisinopril 20 mg daily, furosemide 40 mg
daily, spironolactone 25 mg daily, carvedilol 6.25 mg BID.
Lab results: Na 122, K 2.5, Cl 82, CO2 17, BUN 18, Cr 0.9, glucose 488, ketones
0.1, EKG: heart block, T-wave inversions
Which of the following are contributing to hypokalemia?
0.9% NaCl infusion with IV KCL 40mEq IV x 4 doses
67 you M with CHF and DM 2 presents to ED with N/V, muscle cramps.
Home meds: Lantus 30 mg SQ QHS, lisinopril 20 mg daily, furosemide 40 mg
daily, spironolactone 25 mg daily, carvedilol 6.25 mg BID.
Lab results: Na 122, K 2.5, Cl 82, CO2 17, BUN 18, Cr 0.9, glucose 488, ketones
0.1, EKG: heart block, T-wave inversions
What is most appropriate to administer FIRST?
magnesium
67 you M with CHF and DM 2 presents to ED with N/V, muscle cramps.
Home meds: Lantus 30 mg SQ QHS, lisinopril 20 mg daily, furosemide 40 mg
daily, spironolactone 25 mg daily, carvedilol 6.25 mg BID.
Lab results: Na 122, K 2.5, Cl 82, CO2 17, BUN 18, Cr 0.9, glucose 488, ketones
0.1, EKG: heart block, T-wave inversions
Which other electrolyte should be checked and repleted prn?
Na, K, Mg, Glucose, EKG, Every 4 hours
67 you M with CHF and DM 2 presents to ED with N/V, muscle cramps.
Home meds: Lantus 30 mg SQ QHS, lisinopril 20 mg daily, furosemide 40 mg
daily, spironolactone 25 mg daily, carvedilol 6.25 mg BID.
Lab results: Na 122, K 2.5, Cl 82, CO2 17, BUN 18, Cr 0.9, glucose 488, ketones
0.1, EKG: heart block, T-wave inversions
What should be monitored and how frequently?
hyperkalemia
plasma K+ concentration > 5 mEq/L
rare in patients with normal K excretion, most often seen in renal failure
mild hyperkalemia
serum K + 5-6 mEq/L
moderate hyperkalemia
serum K+ 6.1-6.9 mEq/L
severe hyperkalemia
serum K+ > 7 mEq/L
hyperkalemia primary causes
increaed K intake
decreased K excretion
tubular unresponsiveness to aldosterone
redistribution of K into the ECF
potassium sparing diuretics (spironolactone, triamterene, amiloride)
hyperkalemia caused by tubular unresponsiveness is normally due to ____
potassium sparing diuretics, NSAIDs, ACEI, ARBs
medications that cause hyperkalemia drug induced reduced potassium excretion
hyperkalemia clinical manifestations
acute is more dangerous than chronic
frequently asymptomatic- heart palpitations, skipped heartbeats
severe hyperkalemia: muscle weakness, ECG changes, peaked T waves
IV calcium gluconate
1st line treatment for hyperkalemia with ECG changes
antagonism of the cardiac membrane actions of k+ (stabilize the heart)
temporary hyperkalemia treatments
drive extracellular K+ into the cell
insulin and glucose
sodium bicarbonate, primarily if metbaolic acidosis
B2 adrenergic agonist (albuterol)
hyperkalemia treatment to removal K from body
loop or thiazide diuretics (via kidneys)
cation exchange resin (via GI)
dialysis, preferably hemodialysis if severe
calcium
used in treatment of hyperkalemia
antagonism of membrane actions of K+
antagonizes cardiac membrane effects of hyperkalemia
reverses ECG changes within mins
indicated in patients with significant ECG changes
gluconate preferred over chloride → because chloride associated with tissue necrosis if extravasation occurs
duration of action 30-60 min
no effect on potassium levles ******
IV calcium gluconate dose
1g (one 10ml ampule) IV bolus over 5-10 minutes
insulin and glucose
hyperkalemia treatment
drives extracellular K into the cells (transient effect)
increase activity of Na/K/ATPase pump to drive K intracellular
effect seen in 15 minutes
peaks at 60 min, duration several hours
temporary lowering of plasma K+*******
insulin and glucose dose for hyperkalemia
5-10 units of insulin IV
Dextrose: 50ml ampule of 50%
sodium bicarbonate
treatment for hyperkalemia
drives extracellular K into the cells (transient effect)
preferred treatment in hyperkalemic patients with a metabolic acidosis (low pH, low bicarbonate)
dose: 50-100 mEq infused over 2-5 min
effect begins within 30-60 min
temporary lowering of plasma K
beta 2 adrenergic agonist (albuterol)
hyperkalemia treatment
drives extracellular K into cells (transient effect)
MOA- stimulates Na/K/ATPase pump, stimualtes pacnreatic B receptors to increase insulin release
adjunctive therapy for patients already receiving insulin and dextrose ***
temporary lowering of plasma K+
albuterol dosing for hyperkalemia
10-20 mg in 4 ml of saline by inhalation over 10 minutes
sodium zirconium cyclosilicate (Lokelma)
hyperkalemia treatment
removal of K from the body
no sorbitol content
onset of action: 1 hr
drug interactions: separate adminsitration of other medication by at least 2 hours
sodium polysteren sulfonate (Kayexalate)
hyperkalemia treatment
removal of K from the bdoy
onset 1 hour
separation administration of other medication by at least 6 hours
Patiromer calciium sorbitex (Veltessa)
hyperkalemia treatment
removal of K from the body
onset of action: hours to days
not recommended acute treatment of hyperkalemia
loop diuretics
hyperkalemia treatment
removal of K from the body
promote urinary excretion of K+
dose: Furosemide 20-40 mg IV or PO, titrate to response
losartan, triamterene, CKD stage IV, bactrim
58 yo F with HTN, CKD stage IV presents with weakness, palpitations. She recently
started Bactrim DS for a UTI.
Home meds: Bactrim DS daily, losartan 50 mg, triamterene 50 mg BID.
Labs: Na 135, K 6.2, Cl 108, CO2 20, BUN 52, Cr 3.2, glucose 106. Ca 9.5.
EKG: peaked T waves
What is contributing to her electrolyte disorder?
calcium gluconate
58 yo F with HTN, CKD stage IV presents with weakness, palpitations. She recently
started Bactrim DS for a UTI.
Home meds: Bactrim DS daily, losartan 50 mg, triamterene 50 mg BID.
Labs: Na 135, K 6.2, Cl 92, CO2 20, BUN 52, Cr 3.2, glucose 106. Ca 9.5.
EKG: peaked T waves
After holding home meds, what should be administered FIRST?
insulin and dextrose
58 yo F with HTN, CKD stage IV presents with weakness, palpitations. She recently
started Bactrim DS for a UTI.
Home meds: Bactrim DS daily, losartan 50 mg, triamterene 50 mg BID.
Labs: Na 135, K 6.2, Cl 92, CO2 20, BUN 52, Cr 3.2, glucose 106. Ca 9.5.
EKG: peaked T waves
Which option does NOT remove potassium from the body?
separate form other medications by at least 2 hours
58 yo F with HTN, CKD stage IV presents with weakness, palpitations. She recently
started Bactrim DS for a UTI.
Home meds: Bactrim DS daily, losartan 50 mg, triamterene 50 mg BID.
Labs: Na 135, K 6.2, Cl 92, CO2 20, BUN 52, Cr 3.2, glucose 106. Ca 9.5.
EKG: peaked T waves
Which is an important counseling point about cation exchange resins, like Lokelma?