Hypo Kale Mia

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Hypokalemia 1

Hypokalemia

Hypokalemia is characterized by a serum K concentration of less than 3.5 mEq/L.Ninety-eight percent of K is intracellular.

I.Pathophysiology of Hypokalemia

A.

Cellular Redistribution of Potassium.

Hypokalemia may result from theintracellular shift of potassium by insulin, beta-2 agonist drugs, stressinduced catecholamine release, thyrotoxic periodic paralysis, andalkalosis-induced shift (metabolic or respiratory).B.

Nonrenal Potassium Loss

1.Gastrointestinal loss can be caused by diarrhea, laxative abuse, villousadenoma, biliary drainage, enteric fistula, clay ingestion, potassiumbinding resin ingestion, or nasogastric suction.2.Sweating, prolonged low potassium ingestion, hemodialysis andperitoneal dialysis may also cause nonrenal potassium loss.C.

Renal Potassium Loss

1.

Hypertensive High Renin States.

Malignant hypertension, renal arterystenosis, renin-producing tumors.2.

Hypertensive Low Renin, High Aldosterone States.

Primaryhyperaldosteronism (adenoma or hyperplasia).3.

Hypertensive Low Renin, Low Aldosterone States.

Congenitaladrenal hyperplasia (11 or 17 hydroxylase deficiency), Cushing'ssyndrome or disease, exogenous mineralocorticoids (Florinef, licorice,chewing tobacco), Liddle's syndrome.4.

Normotensive

States

a.

Metabolic acidosis.

Renal tubular acidosis (type I or II)b.

Metabolic alkalosis (urine chloride <10 mEq/day).

Vomitingc.

Metabolic alkalosis (urine chloride >10 mEq/day).

Bartter'ssyndrome, diuretics, magnesium depletion, normotensivehyperaldosteronism5.

Drugs

associated with potassium loss include

amphotericin B,

2 Hypokalemia

ticarcillin, piperacillin, and loop diuretics.II.

Clinical Effects of Hypokalemia

A.

Cardiac Effects

. The most lethal consequence of hypokalemia is cardiacarrhythmias. Electrocardiographic effects include depressed ST seg-ments, decreased T-wave amplitude, U waves, and a prolonged QT-Uinterval.B.

Musculoskeletal Effects.

The initial manifestation of K depletion ismuscle weakness, which can lead to paralysis. In severe cases,respiratory muscle paralysis may occur.

C.Gastrointestinal Effects.

Nausea, vomiting, constipation, and paralyticileus may develop.III.

Diagnostic

Evaluation

A.The 24-hour urinary potassium excretion should be measured.B.If >20 mEq/day, excessive urinary K loss is the cause. If <20 mEq/d, lowK intake, or non-urinary K loss is the cause.C.In patients with excessive renal K loss and hypertension, plasma reninand aldosterone should be measured to differentiate adrenal from non-adrenal causes of hyperaldosteronism.D.If hypertension is absent and patient is acidotic, renal tubular acidosisshould be considered.E.If hypertension is absent and serum pH is normal to alkalotic, a high urinechloride (>10 mEq/d) suggests hypokalemia secondary to diuretics orBartter's syndrome. A low urine chloride (<10 mEq/d) suggests vomiting.IV.

Emergency Treatment of Hypokalemia

A.

Estimated Potassium Deficit

1.At a serum K <3 mEq/L, there is a K deficit of more than 300 mEq2.At a serum K <2 mEq/L, there is a K deficit of more than 700 mEqB.

Indications for Urgent Replacement.

Electrocardiographic abnormalitiesconsistent with severe K depletion, myocardial infarction, hypoxia, digitalisintoxication, marked muscle weakness, or respiratory muscle paralysis.

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