Hypokalemia

Transcellular shifts

• Alkalemia. insulin, catecholamines, hypokalemic periodic paralysis (Ca channelopathy).

acute * in hematopoiesis (eg. megaloblastic anemia treated with Bii, AML crisis) Gl potassium losses (U* < 25 mEq d or <15 mEq L orTTKG <3)

• Gl losses plus metabolic acidosis: diarrhea, laxative abuse, villous adenoma

• Vomiting & NGT drainage usually manifest as renal losses due to 2° hyperaldo & met. alk.

Renal potassium losses (Uk >30 mEq d or >15 mEq L orTTKG >7)

• Hypo- or normotensive acidosis: DKA, RTA (type IV RTA and some type I RTA cause hyperkalemia) alkalosis diuretics, vomiting NGT drainage (via 2° hyperaldosteronism) Bartter's syndrome (loop of Henle dysfxn furosemide-like effect; NEJM 1999.340:1177) Gitel man's syndrome (distal convoluted tubule dysfxn -* thiazide-like effect) Mg depletion: mechanism unclear, variable acid-base

• Hypertensive: mineralocorticoid excess

T hyperaldosteronism (eg.Conns syndrome)

2° hyperaldosteronism (eg. renovascular disease, renin-secreting tumor) nonaldosterone mineralocorticoid (eg. Cushing's. Liddle's. exogenous mineralocort.)

Clinical manifestations

• Nausea, vomiting, weakness, muscle cramps

• ECG: U waves. t 1 QT interval, ventricular ectopy (PVCs. VT. VF)

Workup (NEJM 199&339 4S1)

• Rule-out transcellular shifts

• ✓ 24-hr UK and transtubular potassium gradient (TTKG) = (Uk Pk) (U<*m P^)

U< -30 mEq d or >15 mEq L orTTKG >7 renal loss Uk <25 mEq d or <15 mEq L orTTKG • 3 • extrarenal loss

Figure 4-6 Approach to hjrpokatema

Hypokalemia

It, <25 mEq,'d

UK >30 mEq/d

TTKG <3

TTKG >7

*

*

j Gl Losses| 1

/ \ hypo- or normotensive hypertensive * A

Diarrhea Laxatives Villous adenoma

s acid base status 1" hyperaldo

/ I \ 20 hyperaldo ' ' ^ Non-aldo mmeralo

aademic variable atkalemic

*

* »

DKA

Mgflefic Diuretics * Vomitin^NGT

Bartter's, Gitefman's

• If true potassium deficit potassium repletion (i 1 mEq L 200 mEq total body loss)

KCI 40 mEq PO q4-6h if nonurgent, KCI 10 mEq h IV if urgent, recheck K freq

• Beware of excessive potassium repletion if transcellular shift cause of hypokalemia

• Treat underlying cause (if hydration needed, avoid dextrose-containing solutions as dextrose -» Î insulin intracellular potassium shifts)

• Replete Mg as necessary

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