Martin | Electrolyte Flipped Class

what is the normal serum concentration of potassium?

3.5-5 mEq/L

what is the major physiologic function of potassium?

help with electrical action potential across cell membranes

where is potassium mostly found?

inside the cell

what is the primary route of potassium elimination?

the kidney!

define hypokalemia

K <3.5

what is mild hypokalemia

3.1-3.4

what is moderate hypokalemia

2.5-3.0

what is severe hypokalemia

<2.5

what are common meds that cause hypokalemia?

loop and thiazide diuretics

when do we normally see hypokalemia?

in vomiting or diarrhea

what is the effect of metabolic alkalosis on potassium?

causes an intracellular shift

hypomagnesemia can cause _______

hypokalemia

how do we treat hypokalemia?

potassium replacement

10 mEq of K+ supplementation results in _____ serum increase

0.1 mEq

what is the max oral dose of potassium?

40 mEq per dose

what is the max peripheral IV rate of potassium?

10 mEq/hr

what is the max rate of K+ in a central IV line?

20 mEq/hr

what is the most effective way to treat hypokalemia?

treat multiple electrolyte abnormalities

define hyperkalemia

K > 5mEq/L

what is mild hyperkalemia

5.1-5.9

what is moderate hyperkalemia?

6-7

what is severe hyperkalemia?

>7

what is EMERGENT hyperkalemia?

any level of potassium with EKG changes

what are 4 primary causes of hyperkalemia?

increased intake, decreased excretion, unresponsiveness to aldosterone, redistribution into cellular space

brand name for sodium zirconium cyclosilicate?

Lokelma

brand name of sodium polystyrene sulfonate

kayexalate

how do we treat non-emergent hyperkalemia?

-correct the underlying cause

-loop diuretics

-ion exchange resins

what is Kayexalate’s black box warning?

increased risk of colonic necrosis

how do we treat emergent hyperkalemia?

1. Stabilize cardiac memebranemembrane (calcium)

2. shift potassium to the intracellular space (insulin + glucose, Beta agonitsis, sodium bicarbonate)

3. facilitate removal of potassium (potassium resin binders, potassium-wasting diuretics)

how do we stabilize cardiac membrane in emergent hyperkalemia?

1-2 g calcium over 5-10 minutes

how do we shift potassium into the cell?

-Insulin regular 10 units with IV with 25 g dextrose

-albuterol 10-20 mg nebulized over 10 min

-sodium bicarbonate 50 mEq IV

How can we facilitate potassium removal?

1.Diuretics should be used in patients with preserved renal function

2.Ion exchangers (sodium zirconium cyclosilicate, patiromer, sodium polystyrene sulfonate)

3.dialysis

what is normal range for magnesium

1.7-2.3

_____ can have a profound magnesium wasting effect.

loop diuretics

define hypomagnesemia

< 1.7 mg/dL

what are common medications that cause hypomagnesemia?

diuretics, PPIs, aminoglycosides, digoxin, and nephrotoxic agents

what are s/s of hypomagnesemia?

tetany, twitching, cardiac arrhythmias, chvostek sign, trousseau sign

what is the dose limiting effect of oral magnesium supplementation

diarrhea

what is the side effects of IV mag supplementation

hypotension, flushing, sweating

what is the rate of IV mag supplementation?

1 gram over 1 hour

what is the dose of mag supplementation for hypomagnesemia?

severe depletion (<1.2 mg): 4-6 g administered in divided doses over 12-24 hr

1.2-1.6 mg/dL: 2-4 g

1.6-1.9 mg/dL:1-2

define hypermagnesemia

> 2.4 mg/dL

what is the most common cause of hypermagnesemia?

renal dysfunction

where do we see increased risk of hypermagnesemia?

eclampsia treatment

What are the s/s of hypermagnesemai?

hypotension, bradycardia, reduced deep tendon reflexes, hypotonia

severe: heart block, muscle paralysis, muscle paralysis, respiratory depression

what are the three primary means of treating hypermagnesemia?

1.reduce magnesium intake

2.enhance elimination (loop diuretics)

3.antagonize the physiologic effects of magnesium (reserved for severe, IV calcium 100-200 mg of elemental calcium)

what is the normal range of phosphorus?

2.7-4.5 mg/dL

Phosphorus is a critical component of ____

cellular function (ATP, cell wall, proteins)

what is the major regulator of phosphorus elimination ?

kidneys

what directly inhibits phosphorus reabsorption?

PTH

define hypophosphatemia

< 2.7 mg/dL

what are the common causes of reduced GI absorption?

Cation containing antacids that prevent absorption

hyperparathyroidism and diuretics, malnourished patients who receive rapid refeeding, alcohol use disorder

define hyperphosphatemia

> 4.5 mg/dL

what is the most common cause of hyperphosphatemia?

renal tubular excretion due to CDK/AKI

what are s/s of hyperphosphatemia?

n/v, diarrhea, lethargy, seizures, red eye, pruritus, calciphylaxis and tissue necrosis

how do we treat hyperphosphatemia?

decrease phosphate absorption from the GI tract

what are cation phosphate binders?

calcium, lanthanum, magnesium, iron, aluminum

what are non-cation phosphate binders?

sevelamer, tenapanor

what is the normal range for clacium?

8.6-10.2

how do we calculate a corrected Ca

Corrected Ca= measured Ca+0.8x[4-measured albumin])

PTH ____ calcium levels

increase

define hypocalcemia

Corrected Ca < 8.6 mg/dL

what is the primary cause of hypomagnesemia?

hypoparathyroidism and vit D deficiency

hypomagnesemia is associated with ______

hypocalcemia and hypokalemia

how do we treat hypocalcemia?

severe (<4 mg/dL): 0.5-1 g CaCl OR 3 g of calcium gluconate

mild-moderate: 1-2 g Ca gluconate at a rate of 1 g/hr

CaCl contains ____ amount of elemental calcium than compared to Ca gluconate

3x

what do we avoid rapid administration of calcium?

can lead to severe cardiac dysfunction, including v fib.

what is the max dose of calcemia?

500 mg per dose due to absorption