Info
🌱 來自: Huppert’s Notes
Potassium🚧 施工中
Potassium
Potassium regulation (K**+** 3.5–5.0 mEq/L)
• Distribution:
- 98% intracellular, maintained by Na+/K+ ATPase
• Extracellular K+ shift:
- Acidosis (especially without anion gap)
- Alpha adrenergic stimulation
- Hypertonicity
- Intracellular release (rhabdomyolysis, hemolysis, TLS)
• Intracellular K+ shift:
- Insulin
- Alkalosis
- Beta-2 adrenergic agonists (via Na+/K+ ATPase)
• Secretion of K+: Via ROMK transporter, driven by voltage created from sodium reabsorption in the distal nephron
- Aldosterone: Increases sodium reabsorption via ENac transporter in the distal nephron, increasing potassium excretion
- Volume expansion: Increases distal nephron sodium delivery, but is usually compensated by decrease in aldosterone, which negates the effect on serum potassium level
- Magnesium: Inhibits loss of potassium in the distal nephron in the absence of aldosterone
Hypokalemia (K**+** <3.5 mEq/L)
• Etiology:
- Intracellular shift:
• Insulin and beta-2 adrenergic stimulation are most common
• Other causes include hypothermia, alkalemia, increased blood cell production, barium, chloroquine, cesium, hypokalemic periodic paralysis
- Extrarenal losses (transtubular potassium gradient [TTKG] <3 or urine K <20 mEq/day):
• Diarrhea or other fecal loss. Less commonly profuse sweating.
- Renal losses (TTKG >7 or urine K >20 mEq/day):
• Excess mineralocorticoid activity: Primary hyperaldosteronism, renin-secreting tumor, renovascular disease, Liddle’s syndrome, licorice
• Increased distal-tubule sodium delivery:
- Alkalemic: Emesis, nasogastric suction, diuretics, Barter’s, Gittleman’s
- Acidemic: Renal tubular acidosis, diabetic ketoacidosis (after treatment with insulin)
• Hypomagnesemia
• Amphotericin
• Clinical features:
- Arrhythmias (prolonged conduction, U waves, flattened T waves; can have normal ECG)
- Muscular: Weakness, ileus, rhabdomyolysis
• Diagnosis:
- Step 1: Repeat serum K+ and check Mg2+
- Step 2: Assess volume and acid–base status
- Step 3: Rule out common causes of cellular potassium shift (see potassium regulation section above) by history
- Step 4: Obtain transtubular potassium gradient (TTKG) = [Urine K / Plasma K] × [Plasma Osm / Urine Osm] to help differentiate extrarenal vs. renal losses
• Pearl: Normal urinary K excretion has significant circadian variation, limiting utility of spot urine K measurement
• Treatment:
- Potassium repletion
• Mild: Oral potassium repletion
• Severe: IV potassium repletion
- Do not give more than 20 mEq/hr via central line or 10 mEq/hr via peripheral line, as it is very irritating to blood vessels
- Avoid dextrose-containing solutions which will cause intracellular K+ shift precipitated by insulin release
• Rule of thumb: 10 mEq KCl → increase of 0.1 mEq/L serum K+, replete with half as much potassium in the setting of renal dysfunction
- Treat underlying cause; stop medications that exacerbate hypokalemia if possible (e.g., diuretics, amphotericin B)
- Must treat hypomagnesemia as well
Hyperkalemia (K**+** >5.0 mEq/L)
• Etiology:
- AKI or CKD (usually eGFR <20 mL/min/1.73 m2)
- Spurious: Hemolysis due to tourniquet, small-bore needles, mechanical trauma
- Extracellular shift: Tissue injury (hemolysis, tumor lysis, rhabdomyolysis), acidosis (especially non-anion gap metabolic acidosis), alpha adrenergic stimulation, hypertonicity
- Medications: ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, calcineurin inhibitors, trimethoprim, beta blockers
- Hyporeninemic hypoaldosteronism: Diabetic nephropathy, interstitial renal disease
- Tubular disease: SLE, sickle cell, chronic urinary obstruction, amyloidosis, post-transplant
- Primary adrenal insufficiency
• Clinical features:
- Paresthesias, fasciculations, weakness, paralysis
- EKG changes
• Evolution of EKG changes with increasing hyperkalemia (rate of K+ change more important than K+ concentration): Peaked T wave → ST depression → PR prolongation and P wave flattening → QRS widening → “Sine wave” → Vfib or asystole
• An EKG can be normal minutes before a fatal arrhythmia! A normal EKG should not slow treatment.
• Treatment: “C BIG K Drop”
- Calcium gluconate – Stabilizes myocardial membrane (careful if patient on digoxin). Effect lasts for up to 1 hour.
- Beta-agonist (usually 10 mg of nebulized albuterol)
- Bicarbonate (increases pH) – Shifts K+ into cells, quick fix
- Insulin / Glucose – Requires frequent subsequent glucose measurement, especially in patients with impaired renal function (and decreased insulin excretion).
- Kayexalate (sodium polystyrene sulfonate) – Salt which binds potassium in the intestinal lumen, preventing absorption. Usually works over hours to days. Has risk of GI complications in patients with ileus, colitis, or with prolonged administration. If available, patiromer or zirconium cyclosilicate are safer alternatives.
- Diuretic (Loop diuretic, e.g., furosemide) – Causes urinary loss of potassium
- Dialysis – Used in ESRD, severe AKI or emergent cardiotoxicity