Fluid and Electrolyte Disorders - Potassium and Magnesium

normal serum levels for potassium:

3.5-5.0 mEq/L

normal magnesium levels:

1.7-2.4 mg/dL

start ~50% of usual replacement; the kidneys clear K⁺ and Mg²⁺.

renal dysfunction

use adjusted body weight (AdjBW) for weight-based dosing: AdjBW = IBW + 0.25 × (actual − IBW)

obesity

replace more quickly (but still safely).

acute electrolyte disorders

go slower; the body adapted—rapid correction risks arrhythmias or neuro issues.

chronic electrolyte disorders

the most abundant intracellular cation. serum is tiny (3.5-5 mEq/L) vs intracellular ~150 mEq/L. so small serum moves can represent big total-body changes.

main jobs: sets the resting membrane potential → muscle/nerve excitability; supports metabolism and protein/glycogen synthesis.

potassium

keeps K⁺ inside cells (3 Na⁺ out, 2 K⁺ in, ATP needed).

Na⁺/K⁺-ATPase pump

insulin, β-agonist/catecholamines, alkalosis (H⁺ leaves cells, K⁺ enters to balance charge).

intracellular shift (↓serum K⁺)

acidosis (H⁺ enters, K⁺ exits), hyperosmolality (water leaves cells → K⁺ follows), cell lysis, aldosterone deficiency.

(↑serum K⁺)

potassium:

absorption: upper GIT.

excretion: kidney ~80%, GIT ~15%. ____________________ stimulates urinary K⁺ excretion—think diuretics and RAAS.

aldosterone

stimulates Na⁺/K⁺-ATPase → lowers serum K⁺.

insulin

same pump, plus boosts insulin → lowers K⁺.

catecholamines (β-activity)

renal K⁺ wasting → lowers K⁺.

aldosterone

H⁺ in, K⁺ out via H⁺/K⁺ ATPase → raises K⁺.

acidosis (low pH)

cell shrinks, K⁺ leaves → raises K⁺.

hyperosmolality

H⁺ moves into cells to be buffered → K⁺ moves out → ↑ serum K⁺.

acidosis

H⁺ leaves cells → K⁺ moves in → ↓ serum K⁺.

alkalosis

K⁺ < 3.5 mEq/L.

hypokalemia

select all that apply:

what are some common causes of hypokalemia?

1. poor intake

2. GI losses

3. renal losses

4. altered distribution

5. skin losses

select all that apply:

what is the initial management approach for hypokalemia?

1. assess severity + symptoms + EKG

2. fix magnesium first or alongside if low

3. choose route & product

4. treat the cause

H⁺ moves into cells to be buffered → K⁺ moves out to keep charge balanced → serum K⁺ rises (sometimes "normal" despite big total-body losses, e.g., DKA).

acidosis (↑H⁺ in blood)

H⁺ leaves cells → K⁺ moves into cells → serum K⁺ falls.

alkalosis (↓H⁺ in blood)

super common electrolyte issue. usually reflects total-body K⁺ depletion. not typical in healthy adults unless there's loss (GI/renal) or shift (into cells). up to ~50% of patients on loop or thiazide diuretics will run low at some point.

hypokalemia

select all that apply:

what are some clinical manifestations of hypokalemia?

1. ECG changes progress with lower K⁺

2. weakness, cramps, paralysis

3. rhabdomyolysis

4. intestinal ileus

helps maintenance, not rescue: bananas, oranges, tomatoes, potatoes, avocado; salt substitutes (KCl) if safe.

diet

workhorse; fixes diuretic/diarrhea-type losses and metabolic alkalosis

KCl

choose when phosphate is also low.

K-phosphate

helpful in metabolic acidosis or renal tubular acidosis.

all of the above

microencapsulated better tolerated; wax matrix = more GI erosions

sustained-release tabs/caps

work fastest but taste tragic; often contain sorbitol → diarrhea risk.

liquids

split doses. >40 mEq/day → divide (e.g., 20 mEq BID or 20 mEq TID).

GI tolerance

select all that apply:

what is the typical parenteral potassium dosing?

1. prevention: ~20 mEq/day

2. typical treatment: 40-100 mEq/day split

3. expect ~0.1 mEq/L rise per 10 mEq KCl

select all that apply:

what are some safety concerns with parenteral potassium dosing compared to oral?

1. pain/phlebitis

2. arrhythmias/hyperkalemia

select all that apply:

when do you use an IV for potassium?

1. severe (

select all that apply:

what are the general rules for parenteral potassium dosing?

1. heuristic: 10 mEq IV KCl → ~↑0.1 mEq/L

2. cut dose ~50% in renal impairment

select all that apply:

which of the following apply to parenteral potassium preparation and administration?

1. use NaCl-containing fluid

2. peripheral: max 10 mEq per 100 mL

3. central: can concentrate to 40 mEq in 100 mL.

select all that apply:

what are the infusion rates in parenteral potassium preparation and administration?

1. ≤10 mEq/hr → peripheral no cardiac monitor

2. >10 mEq/hr up to 20 mEq/hr → central, cardiac monitoring

use to reduce renal wasting when diuretics are necessary or in hyperaldosteronism.

potassium-sparing diuretics

(aldosterone antagonist) - watch for gynecomastia, hyperK.

spironolactone

can be used if gynecomastia an issue

eplerenone

select all that apply:

which of the following are direct ENaC blockers?

1. amiloride

2. triamterene

potassium sparing diuretics are often added to loop/thiazide regimens or when _________________ is chewing up K⁺.

amphotericin B

select all that apply:

why does NS drip lower K⁺?

1. chloride load

2. mild metabolic acidosis at kidney level

3. RAAS kick

4. ↑aldosterone

why is insulin listed as a cause of hypokalemia?

it drives K⁺ into cells via Na⁺/K⁺-ATPase; dextrose co-admin can worsen the shift.

select all that apply:

what do we need to monitor in potassium IV therapy?

1. serum K⁺

2. look for phlebitis

3. look for infiltration/extravasation

4. any rate >10 mEq/hr needs cardiac monitoring

5. never bolus KCl

how would you monitor a patient undergoing chronic diuretic therapy and taking potassium orally?

check K⁺, Mg²⁺, and renal function every 1-2 months, sooner if dose changes or symptoms.

how do we monitor a patient that is hospital with mild hypokalemia managed with oral potassium?

check K⁺ q2-3 days. you should see a bump within 72 h; no rise = suspect low Mg²⁺ or ongoing loss (diarrhea, diuretic).

if moderate-severe hypomagnesemia, fix Mg²⁺_______________.

first

K⁺ >5.0 mEq/L. less common, but more likely to kill quickly.

hyperkalemia

select all that apply:

what are some causes of hyperkalemia?

1. hemolyzed specimen

2. excessive intake

3. shift out of cells

4. excretion failure

what is the clinical manifestation of hyperkalemia?

ECG changes progress: peaked T → PR/QRS prolongation → sine wave → VF/asystole, and weakness/paralysis

select all that apply:

what are some non-pharmacological therapies for hyperkalemia?

1. diet education

2. medications

3. dialysis

4. hemofiltration therapy

select all that apply:

when do you use when K⁺ ≥6.0 or ECG changes or symptomatic?

1. stabilize myocardium

2. shift K⁺ back into cells

3. remove K⁺ from the body

select all that apply:

which of the following should be stopped when the patient has hyperkalemia?

1. halt all K⁺ sources

2. IV fluids with K⁺

3. TPN

4. oral supplements

5. K-sparing meds

select all that apply:

how do we treat hyperkalemia at

1. diet + med review

2. consider loop diuretic

3. one binder (SPS/patiromer/SZC)

select all that apply:

how do we treat ≥6.0 or ECG changes?

1. calcium gluconate

2. insulin+dextrose

3. albuterol

4. bicarb if acidotic)

5. elimination (loop, binder, or dialysis).

with a ____________________ IV, calcium gluconate is preferred over calcium chloride.

peripheral

select all that apply:

how do we monitor mild-moderate hyperkalemia?

1. normal kidneys: check K⁺/SCr monthly

2. renal dysfunction: check q2 weeks

select all that apply:

how do we monitor acute symptomatic hypernatremia?

1. continuous ECG until K⁺ < 5.0 mEq/L

2. serum K⁺ q1-6h

3. medication reconciliation for culprits

4. treatment-specific monitoring

2nd most abundant intracellular cation. absorbed mainly in the jejunum; cleared by kidneys.

magnesium

select all that apply:

what are some roles of magnesium?

1. enzyme cofactor everywhere

2. natural calcium channel blocker

3. stabilizes neuromuscular/cardiac excitability

4. supports K⁺ retention

clinically we like Mg around:

~1.7-2.4 mg/dL

if K⁺ is low and won't correct, fix Mg²⁺ first. no Mg²⁺ →____________ leaks K⁺.

kidney

Mg < 1.7 mg/dL

hypomagnesemia

select all that apply:

what are some symptoms of hypomagnesemia?

1. refractory hypokalemia and often hypocalcemia

2. hyperreflexia, tremor, cramps

3. tetany, seizures, coma if severe

4. prolonged PR and QT, U waves

5. risk of torsades and other arrhythmias

select all that apply:

what are some causes of hypomagnesemia?

1. low in / poor absorption

2. renal wasting

3. shift into cells

4. RRT (dialysis)

long-term ___________________ use can cause Mg wasting (likely impaired intestinal absorption)

proton pump inhibitors

Mg may stay low despite supplements until the PPI is stopped; not an issue with ___________________ like famotidine.

H₂ blockers

select all that apply:

what would you give a hypomagnesemic patient that can take oral magnesium?

1. magnesium oxide

2. Mg hydroxide/citrate, gluconate, lactate, carbonate

3. separate by 2 hours from other meds

4. use PO for maintenance

select all that apply:

how do we treat hypomagnesemia with parenteral methods?

1. 1 g MgSO₄ (≈ 8 mEq) raises serum Mg ~0.1 mg/dL

2. halve the dose in renal impairment

3. infusion rate: ≤8 mEq/hr (≈ 1 g/hr)

select all that apply:

how do we monitor hypomagnesemia therapy?

1. PO: watch GI tolerance

2. IV, mild-moderate (asymptomatic): check daily

3. IV, symptomatic/severe: check q1-6 h initially

4. IV, severe: check daily once stabilized

PO Mg oxide 400 mg TID (adjust to stools) + recheck in 24-48 h. If on a PPI, consider step-down/stop.

hypoMg (no symptoms, Mg 1.3-1.6)

MgSO₄ 2 g IV now, then 2-6 g IV over 3-6 h depending on ECG and renal function; repeat labs in 4-6 h; start PO maintenance next day if able.

hypoMg (symptomatic or Mg ≤1.2)

telemetry on → calcium if ECG changes → insulin + D50 ± albuterol ± bicarb if acidotic → start elimination (loop/binder/dialysis) → K⁺ q1-3 h, glucose q1 h x 4-6 → wean monitoring once K⁺

hyperK monitoring script (acute)

Mg > 2.4 mg/dL. clinically significant symptoms usually don't show up until >4-5 mg/dL; >12 mg/dL can be fatal.

hypermagnesemia

select all that apply:

why does hypermagnesemia happen?

1. iatrogenic + impaired kidneys

2. renal failure

3. tumor lysis

Mg is a physiologic __________________ and neuromuscular chill pill. too much → decreased muscle tone and conduction.

calcium antagonist

select all that apply:

what are some symptoms of hypermagnesemia?

1. hypotension

2. bradycardia

3. heart block

4. hyporeflexia

5. muscle weakness

6. paralysis

7. somnolence → coma

select all that apply:

how do we treat hypermagnesemia?

1. stop the source

2. antagonize the toxicity (fast)

3. enhance elimination

4. supportive care