0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 13, 2007 7:54
788 Hypokalemia■KCl is preferred when hypokalemia is accompanied by metabolic
alkalosis
■K citrate or KHCO3 is preferred when accompanied by metabolic
acidosis
■intravenous K may be preferred with symptomatic hypokalemia,
EKG changes, current use of digoxin, or when the patient cannot
take PO
➣K concentration in intravenous solutions should not be >40
mEq/L
➣ECG monitoring is recommended with intravenous K adminis-
tration
■with more life threatening hypokalemia such as paralysis or ventric-
ular arrhythmias
➣concentration >40 mEq/l and infusion of >40 mEq/L may be
indicated
➣such concentrations require access to a central vein,
➣cardiac monitoring absolutely required
■in setting of Mg++deficiency, correction of Mg++deficit is required
to correct K
■redistribution – self limited
■periodic paralysis – acetazolamide
■type I distal renal tubular acidosis – K citrate
■Bartter’s syndrome – KCl, MgCl2, amiloride
■aldosterone producing tumor – surgical removal or spironolactone
■bilateral adrenal hyperplasia – spironolactone
■Liddle’s syndrome – amiloride or triamterene
■glucocorticoid remedial hyperaldosteronism – glucocorticoids
follow-up
■measure K to ensure replacement therapy is effective
■treat hypertension aggressively when present
➣use caution when using angiotensin converting enzyme inhibitor
or angiotensin receptor blocker in setting of oral K or K sparing
diuretics
complications and prognosis
■clinical manifestations of hypokalemia often subtle
■hypokalemia can be complicated by:
➣neuromuscular: weakness, fatigue, paralysis
➣gastrointestinal: constipation
➣renal: polyuria, polydipsia (nephrogenic diabetes insipidus)
➣endocrine: glucose intolerance