Page 1378 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 99: Electrolyte Disorders in Critical Care 951

sodium delivery. Furthermore, resorption of sodium by the principal TABLE 99-4 Causes of Hypokalemia
cells generates a negative charge in the tubular lumen. The luminal
electronegativity enhances potassium secretion. Some of this negative Decreased Potassium
charge is lost by concurrent resorption of chloride. Decreased distal Intake Cellular Shift Increased Potassium Loss
chloride delivery, as occurs with metabolic alkalosis, reduces chloride Anorexia β-Adrenergic activity Extrarenal losses
resorption, thereby increasing the tubule electronegativity and enhanc- Malnutrition/malabsorption Endogenous Chronic diarrhea
ing potassium secretion. Aldosterone is a steroid hormone produced
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in the zona glomerulosa of the adrenal gland. Its principal site of action Alcoholism Albuterol Fistulas and ostomies
is the connecting segment and collecting tubules of the distal nephron. Ingestion of grey clay Dobutamine Renal losses
In the principal cells of the cortical collecting duct (CCD), aldo- Terbutaline Loop diuretics
sterone increases the resorption of sodium and hence the secretion of
potassium. Aldosterone stimulates the production and activity of Na-K- Fenoterol Thiazide diuretics
ATPase, sodium channels, and potassium channels. Aldosterone Insulin Osmotic diuretics
59
also has a small but measurable effect on increasing GI potassium Alkalemia Acetazolamide
excretion. Aldosterone is secreted in response to angiotensin II and
49
elevated serum potassium. Periodic paralysis Type I and II renal tubular
The fact that potassium secretion is dependent on both tubular flow Thyrotoxicosis acidosis
and aldosterone means that urinary potassium excretion is independent Familial Metabolic alkalosis
of volume status despite the fact that both tubular flow and aldosterone
are intimately tied to volume status. With volume depletion, increased Xanthines Bicarbonaturia (vomiting)
angiotensin II stimulates the release of aldosterone, which enhances potas- Theophylline toxicity Ketonuria
sium secretion; however, the simultaneous decrease in GFR and increased Caffeine Hypomagnesemia
resorption by the proximal tubule decrease tubular flow, antagonizing
potassium secretion. In the opposite case of volume overload, decreased Barium toxicity Carbenicillin
aldosterone suppresses potassium secretion, but increased tubular flow Treatment of anemia (rapid Bartter and Gitelman
enhances potassium secretion, maintaining potassium balance. cell proliferation) syndromes
■ HYPOKALEMIA Hyperaldosteronism
Exogenous steroids
Hypokalemia is defined as a serum potassium concentration below Adrenal adenoma
3.5 mmol/L, and is found among 20% of the hospitalized population. Adrenal hyperplasia (Conn
However, this high frequency probably does not reflect total body potas-
sium depletion. In a review of 70 hospitalized patients with a potassium syndrome)
less than 2.8 mmol/L, the potassium rose toward normal regardless if Syndrome of apparent
they were given potassium or not. The authors suggested that hospital- mineralocorticoid excess
ization for acute illness was associated with increased adrenergic stimu- Liddle syndrome
lation, resulting in intracellular movement of potassium and transient Congenital adrenal hyperplasia
hypokalemia. 60
Renal artery stenosis
Etiology: See Table 99-4. Renin-secreting tumor
Decreased Dietary Intake Potassium-poor diets usually are merely contribu-
tory to hypokalemia. In a study of normal individuals, a potassium
restricted diet (20 mmL/day) was associated with a decline in serum potassium excretion. Studies in nephrectomized dogs show a modest
potassium from 4.1 mEq/L to 3.5 mEq/L. Even among patients with but measurable decrease in serum potassium of less than 0.3 mmol/L
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severe malnutrition due to anorexia nervosa and/or bulimia, serum for each increase in pH of 0.1 (though these data did not account for a
66
potassium less than 3 mmol/L occurred in less than 2%, and in all of significant increase in serum osmolality). The common association of
those patients there was enhanced potassium loss from cathartics or alkalosis and hypokalemia is primarily due to enhanced renal excretion
vomiting. 62 of potassium rather than a transmembrane shift.
Hypokalemic periodic paralysis is an unusual clinical entity in which
Cellular Shifts Activation of β-adrenergic receptors increases Na-K-ATPase transcellular shifts in potassium result in paralysis. These patients
activity. Any physiologic stress that releases epinephrine or norepi- develop sudden, severe drops in serum potassium associated with skel-
nephrine can result in a transient decrease in serum potassium. Use of etal muscle paralysis. Triggers include carbohydrate loads, exercise, and
primarily β-adrenergic catecholamines, such as dobutamine, can cause changes in body temperature. Acetazolamide may decrease the frequency
transient hypokalemia. The β-agonists used for bronchodilation or as and severity of symptoms in some families; recent work suggests this
63
tocolytic agents can also acutely lower potassium. response varies according to genotype. 67,68 Oral potassium can be used to
Insulin reliably stimulates Na-K-ATPase and lowers serum potassium. treat acute paralysis but patients often develop rebound hyperkalemia. 69
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Insulin-induced hypokalemia has been documented in the treatment
of diabetic ketoacidosis and hyperosmolar nonketotic states, and with Increased Potassium Loss The cortical collecting duct is the critical site of
the use of intravenous dextrose solutions. Refeeding syndrome occurs renal potassium handling. Normally aldosterone activity and sodium
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among patients given a carbohydrate-rich diet or parenteral nutrition delivery to the CCD are balanced so that when one is elevated the other
following periods of starvation. Refeeding syndrome is associated with is decreased. Excess renal potassium excretion only occurs when both
hypokalemia and hypophosphatemia. 65 aldosterone and distal sodium delivery are increased.
Metabolic (or respiratory) alkalosis is associated with the intracel- Most diuretics increase distal delivery of sodium and increase aldo-
lular movement of potassium. Increased pH results in movement of sterone, resulting in hypokalemia. Primary hyperaldosteronism causes
hydrogen ions from the intracellular to the extracellular compartment. hypertension and hypokalemia. The hypokalemia is due to the simul-
Potassium shifts into cells to maintain electroneutrality. In addition, taneous increase in aldosterone activity and sodium delivery to the
in metabolic alkalosis, increased serum bicarbonate enhances renal distal nephron. The increased sodium delivery is due to a spontaneous

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