K + Mg

Potassium: Physiology and Role

most abundant cation in the body (~3,000 mEq) and is mainly intracellular (98%), with serum levels normally 3.5–5 mEq/L.
Roles: protein/glycogen synthesis, cellular metabolism, regulation of cell membrane electrical action potentials, cardiovascular and neuromuscular function.
Na/K ATPase pump - sustains Potassium gradient across cell membranes

Clinical Manifestation
- Heart: ECG changes, dysrhythmias, conduction defects,
- Muscles: weakness, myalgias, cramps, paresthesias, tetany, and paralysis.
Etiologies
- Excessive renal loss (90% via kidneys) and GI loss (diarrhea, vomiting, laxatives). Medication-related: Diuretics, mineralocorticoids, cation exchange resins
- Intracellular shift from insulin (↑Na/K ATPase activity) or catecholamines stimulating B2 receptors activating the pump or glycogenolysis increasing insulin secretion
- Hypomagnesemia impairs Na/K ATPase, worsening renal K loss
  - correct Mg before K.

	range mEq/L	how KCl replace
Mild	3 - 3.5	PO (tab, cap, liquid)
Moderate	2.5 - 3	IV or PO
Severe	< 2.5	IV aaaaaaaaaaaaaaaaaaaaaaaaaaa if risk of serious symptoms or arrhythmias do IV or PO

IV Supplementation (KAc, KP, KCl)
- prepare in saline since dextrose may stimulate insulin
- max infusion rate = 10 mEq/h never IV push
- ADR - arrhythmia, phlebitis, infusion site pain
Pt Counseling points
- GI intolerance (N/V, abdominal pain) take with food and divide dose
- Full glass of water or juice to dilute do not crush or chew
  - can open capsule and sprinkle contents on soft cool food

Clinical Manifestations
- Heart: ECG changes, dysrhythmias, conduction defects
- Muscle: weakness, twitching, cramps, paralysis
- Kidney: metabolic acidosis
Etiologies
- Excess intake (rare) - K supplementation overcorrection, dietary noncompliance, salt substitutes
- Reduced excretion - Renal failure, hypoaldosteronism (RAAS), medications
  - ACEi/ARBs, K-sparing diuretics, trimethoprim
- Extracellular shift - cell lysis or tumor lysis syndrome, metabolic acidosis, hyperosmolality, insulin deficiency, meds
  - Digoxin, succinylcholine, non-selective Beta blockers,
- Hemolysis - traumatic blood draw causes release of intracellular K causing pseudo-hyperkalemia.
  - check for apparent cause and wide variability in repeated labs

Protect the heart - IV calcium avoiding Na lines for precipitate risk (if ECG changes, not monotherapy)
- gluconate 10% (1-3g) or chloride 10% 0.5-1g) both onset of 1-3 mins and lasts 30-60 min
- gluconate less irritating to conscious Pt but usually underdosed
- chloride higher risk of extravasation and tissue necrosis
Shift K intracellularly - all have onset of 30 min
- regular or rapid Insulin ± dextrose 5-10 units ± 25-50 g dextrose IV (BG <250 mg/dL) lasts 2-6 hr
- albuterol 10-20 mg nebulizer lasts 1-2 hr
- sodium bicarbonate (for acidosis) 50-100 mEq IV lasts 2-6hr
Eliminate K - furosemide or potassium binders
- Furosemide (lasix) 20 - 40 mg IV onset 30 min (renal dep) lasts 4-6 hr
- Potassium Binders aka cation exchangers
  - veltassa/patiromer binds to K in GI lumen to exchange for Ca2+
    - onset 4-7 hour lasts vary
    - ADR - constipation ,nausea, hypomagnesemia, DDI with PO meds should have 3+ hr gap
  - Lokelma binds K+ in Gi lumen to exchange for Na and H
    - onset 1 hour lasts vary
    - ADR: edema, DDI with PO meds leave 2+ hour gap
  - Hemodialysis - most effective, invasive, time consuming for emergency or last line
    - 4 hr dose immediate onset with lasts variable
Monitor electrolytes, volume status, renal function, blood glucose

second most abundant intracellular cation; mostly found in bone (67% and muscle (20%)
- Serum normal: 0.7–1.25 mmol/L or 1.6-2.5 mg/dL. in body 25 g
Roles: Cofactor for numerous enzymatic and biochem reactions (ATP-dependent), cardiovascular and neuromuscular function.

Clinical Manifestations -
- Heart: ECG changes and arrhythmia
- Brain: confusion/delirium, seizures, coma, vertical nystagmus (eye twitches)
- Muscle: weakness, lethargy, tremor, paresthesia (tingling/numbness), tetany (spasms)
- GI: N/V
Etiologies
- Inadequate intake/absorption daily ~ 400g
  - long nasogastric suction, malabsorption, short-bowel syndrome (resection/bypass)
- Excess loss: ~95% of renal filtered reabsorbed or GI loss (N/V/D) or defect in renal reabsorption
  - medication: laxative abuse, diuretics, PPI, aminoglycosides, amphotericin B, cyclosporine, tacrolimus
- Chronic Alcoholism - less intake combined with renal and GI loss

Route	Indication	Replacement
PO	>0.5 mmoL asymptomatic	Mg Oxide 400-800 mg BID
IV	< 0.5 mmoL symptomatic or PO intolerant	Mg sulfate 1 -8 g over 24 hours

Other Po salts available
- gluconate tablet 500 mg
- hydroxide tablet or solution 400 mg or 400 mg/5 mL
- citrate solution 290 mg/5 mL
- lactate tablet (Tab SR) 84 mg reduce diarrhea
- chloride (slow mag) 64 mg reduce diarrhea
- stagger Mg to avoid DDI to decrease absorption of fluoroquinolones, TCA, mycophenolate, bisphosphatase
IV max 2g/hr with 50% excreted in urine
- emergency 2g in 10 mL NS IV push over 1 min
  - will cause flushing sweating and hypotension
- can do IM if IV needed and impossible, but painful

Etiologies - Uncommon, but can occur from renal impairment, overcorrection, or excess Mg-containing antacids/laxatives intake

Antagonize effects - IV calcium gluconate for cardiac/neuromuscular toxicity
Reduce intake - Discontinue exogenous Mg
Promote elimination - IV fluids, loop diuretics, and hemodialysis with some K if severe.