Potassium and Magnesium Abnormalities

what is potassium and its function?

-intracellular cation that has beneficial effects of BP, reduces risk of kidney stones, and decreases bone loss

-essential for cardiac muscle contraction and nerve impulses

-imbalances can lead to fatal cardiac arrythmias and neuromuscular disturbances

what are 3 mechanisms that balance K+ levels in the body?

-intake

-transcellular shifts

-excretion

what are the 3 classifications of hyperkalemia and their associated lab values?

-mild: 5.1-5.9

-moderate: 6-7

-severe: >7

what are 2 characteristics of hyperkalemia epidemiology?

-AKI and CKD are the most common pathophysiological causes

-risk of arrythmias and death increase based on K+ level and rate of change

what are 3 etiologies of hyperkalemia?

-increased intake: rarely a problem for people with normal kidney function

-transcellular shifts: from muscle injury, seizures, acidosis

-decreased excretion/secretion: from aldosterone antagonism or RAAS inhibition

what are 2 factors to be considered related to increased intake of K+?

-can be due to supplementation or medications such as penicillin g potassium

-no specific recommendation to limit K+ intake for patients with CKD

what are 5 factors that can lead to transcellular shifts of K+?

-cell destruction/lysis

-acidosis

-DM

-CKD

-beta blocker use

what are 4 causes of pseudohyperkalemia?

-extravascular hemolysis of RBCs

-leukocytosis

-platelet clotting

-muscle release

what are 5 drugs associated with impaired excretion/secretion of K+?

-RAASi

-NSAIDs

-bactrim, amiloride

-heparins

-tacrolimus

what are 4 aspects of the clinical presentation of hyperkalemia?

-typically asymptomatic

-muscle weakness or heart palpitations

-often identified through abnormal labs

-causes EKG changes, like peaked T waves

what are 2 guidelines that should lead to referral for urgent management?

-K+ > 6 mmol/L with or without EKG changes

-anyone with hyperkalemia and EKG changes

what are 3 suggestions for management of hyperkalemia if the patient does not have EKG changes?

-repeat K+ measurement if pseudohyperkalemia is suspected

-review drug list for offending agents

-rule out urine retention due to obstruction

what are the 3 suggestions for determining urgency of hyperkalemia?

-K+ over 6.5 or K+ over 5.5 with kidney function impairment should lead to immediate reduction

-those going through surgery or with marginal kidney function/UO should lower K+ within 6-12 hr

-chronic elevations due to CKD or medication use should lower K+ over 24 hr+

what are the 3 main aspects of hyperkalemia treatment?

-stabilize myocardium using calc gluconate

-shift serum K+ to intracellular space with insulin, albuterol, or sodium bicarb (only metabolic acidosis patients)

-remove K+ from body with loop diuretics, GI cation exchangers, or HD

what is the MOA, indication, dose, and PK for calcium gluconate?

-antagonize effect of K+ on membrane potential

-severe hyperkalemia with EKG changes

-1-2 g of calc IV over 2-3 min, repeat in 5-10 min if no EKG change

-immediate onset, duration of 30-60 min

what are the main clinical considerations for using calcium gluconate vs calcium chloride?

gluconate has less risk of tissue necrosis with peripheral admin, chloride has 3x elemental calc and central line admin is preferred

what is the MOA, indication, dose, PK, and monitoring for regular insulin and dextrose?

-insulin stimulates Na+/K+/ATP pump, dextrose prevents hypoglycemia

-hyperkalemic emergency

-10 units IV bolus + 50 mL D50W over 5 min

-10-20 min onset, duration of 2-6 hr

-glucose level every 30-60 min for up to 6 hr

what are 2 clinical considerations for use of regular insulin and dextrose?

-omit dextrose if hyperglycemic (>250)

-lower dose by 5 units in AKI or CKD due to decreased clearance

what is the MOA, indication, dose, PK, and monitoring for albuterol?

-stimulates Na+/K+/ATP pump

-hyperkalemia after standard therapy

-10-20 mg via nebulizer over 10 min

-5 min onset, 3-6 hr duration

-HR, BP, tremors, anxiety

what is the MOA, indication, adverse effects, and PK for SZC (lokelma)?

-K+ binder that exchanges K+ for H+ and Na+ in GI lumen

-chronic hyperkalemia, can be used for severe in combination with other treatments

-edema and hypokalemia

-1 hr onset

what are the dosing suggestions for SZC (lokelma)?

-severe: 10 g TID for up to 48 hr

-chronic: 10 g TID for up to 48 hr, followed by 10 g qd

what are 2 clinical considerations for SZC (lokelma)?

-separate dosing from other oral meds by > 2 hr

-avoid use in patients with severe constipation, GI obstruction, or bowel mobility issues

what is the MOA, indication, dose, and PK for PSC (veltassa)?

-K+ binder that exchanges K+ for Ca2+ in GI lumen

-chronic hyperkalemia due to slower onset

-8.4 g qd

-7 hr onset

what are 5 clinical considerations for use of PSC (veltassa)?

-separate dosing from other oral meds by > 3 hr

-can cause constipation and other GI issues

-avoid use in patients with GI issues such as bowel mobility problems

-may cause hypomagnesemia

-do not add to warm liquids or foods

what is the MOA, indication, adverse effects, and PK for SPS (kayexalate)?

-K+ binder that exchanges free K+ for Na+ in GI lumen

-chronic hyperkalemia due to slower onset

-CI for patients with obstructive bowel disease

-2-6 hr onset

what are the dosing recommendations for SPS (kayexalate)?

-oral: 15 g qd-QID

-rectal: 30-50 g q6h

what are 4 clinical considerations for SPS (kayexalate)?

-separate oral dosing of other meds by >3 hr

-avoid use in most patients unless other therapies unavailable

-avoid use in postop patients, CVD, renal impairment, constipation

-do not mix in orange juice or any juice with K+

what are the 3 main monitoring parameters for hyperkalemia?

-EKG: repeat Ca2+ treatment prn to normalize

-glucose: check q30-60min for 4-6 hr if using insulin

-potassium: monitor for hours to days

what are 4 hyperkalemia prevention recommendations for patients with CKD and/or HF?

-avoid fasting

-avoid or reduce use of drugs like NSAIDs; if necessary, use K+ binders and loop or thiazide diuretics

-treat chronic metabolic acidosis with sodium bicarb

-limit K+ intake to whole foods

what are the 3 classifications of hypokalemia and their lab values?

-mild: 3.1-3.5

-moderate: 2.5-3

-severe: <2.5

what are the 3 main etiologies of hypokalemia?

-decreased K+ intake

-transcellular shifts

-increased K+ loss

what are the 3 epidemiologies associated with hypokalemia?

-chronic diarrhea, malnutrition, critical illness

-most common cause is drug induced hypokalemia from loop and thiazide diuretic use

-2nd most common is GI fluid loss

what are 2 pathophysiologies of hypokalemia?

-delays ventricular repolarization

-hypomagnesemia often occurs simultaneously; increases urinary K+ losses and prevents reabsorption

what are 5 symptoms of hypokalemia?

-muscle weakness or cramps

-EKG changes, flattened T waves

-paralysis

-respiratory failure

-cardiac arrythmias

what are 3 results of prolonged hypokalemia?

-increased ammonia production and bicarb reabsorption

-elevated BP

-decreased phosphate reabsorption

what are 3 classes of drugs that can cause hypokalemia and examples of each?

-b2 receptor agonists: epinephrine, albuterol, pseudoephedrine

-diuretics: loop diuretics, thiazides, acetazolamide

-K+ binders: lokelma, patiromer, SPS

what are 4 evaluation points of hypokalemia?

-check for high sodium diet

-check for increased urinary flow

-check for activation of Na+/K+/ATPase

-check for hypovolemia

what are the 3 main treatment steps for hypokalemia?

-check Mg2+ and replete first

-replenish K+ using 40 mEq q4-6h PO

-expect to replete 10 mEq for every 0.1 away from 4

what are the 4 main types of oral potassium supplementation and their differences?

-chloride: most effective for diuretic and diarrhea induced

-gluconate: more palatable than KCl

-phosphate: concurrent hypophosphatemia

-bicarbonate: concurrent metabolic acidosis

what are 3 characteristics of IV potassium supplementation?

-do not administer undiluted or by IV push

-comes as chloride, phosphate, or acetate

-wait >30 min from end of each infusion to recheck

what are the administration directions for 2 routes of IV potassium supplementation?

-peripheral: 10 mmol/100 mL NS over at least an hour

-central line: 20-40 mEq/100 mL at max of 40 mEq/hr

what is magnesium and its main functions?

intracellular cation that is a cofactor for many reactions such as neurotransmission, vascular tone, and cardiac conduction

what are the 4 main etiologies of hypomagnesemia?

-decreased intake due to starvation or alcohol use disorder

-loop and thiazide diuretics or PPIs

-redistribution due to acidosis

-GI and renal losses due to diarrhea or hungry bone syndrome

what are 3 aspects of the pathophysiology of hypomagnesemia?

-hypokalemia due to increased urinary excretion

-hypocalcemia due to decreased PTH release

-risk for cardiac arrhythmias

what are 4 clinical presentations of hypomagnesemia?

-asymptomatic until >1.2 mg/dL

-early presentation includes N/V, fatigue, etc

-can include tremors, seizures, and psychosis

-can lead to Afib and ventricular arrhythmias

what are 5 suggestions for hypomagnesemia treatment?

-treat concurrent hypocalcemia if needed

-asymptomatic, non hospitalized patients should take SR PO meds

-hospitalized patients should take IV

-continue Mg2+ repletion for 1-2 days after serum concentration normalizes, intracellular stores take longer

-use K+ sparing diuretics in those with diuretic induced hypomagnesemia

what are 3 clinical presentations of hypermagnesemia?

-neuromuscular toxicity

-hypotension and bradycardia when over 4.8 mg/dL

-paralysis, heart block when over 12 mg/dL

what are the 3 main treatment steps for hypermagnesemia?

-restore normal kidney function: cessation of Mg2+ therapy and use loop or thiazide diuretics

-moderate kidney impairments: IV isotonic fluids and a loop diuretic

-dialysis, use IV as a Mg2+ antagonist if patient is symptomatic