Hypokalemia clinical significance

Fixed combinations of thiazides and loop diuretics with potassium and of thiazides with beta-blockers serve little useful purpose and can in fact do harm. Combinations of thiazides and loop diuretics with potassium-sparing diuretics serve the needs of the small minority of patients who develop clinically significant hypokalemia when given diuretics alone, or in whom hypokalemia is particularly risky. In fact, these combinations are much too widely used, and since individual needs vary so much there is a spectrum of risk, ranging from hypokalemia to hyperkalemia (SEDA-10, 370) (SEDA-10, 371). 

The concentration of serum electrolytes may also be altered secondary to the development of respiratory alkalosis. The serum chloride concentration is usually slightly increased, and serum potassium concentration may be slightly decreased. Clinically significant hypokalemia can be a consequence of extreme respiratory alkalosis, although the effect is usually very small or negligible. Serum phosphorus concentration may decrease by as much as 1.5 to 2.0 mg/dL because of the shift of inorganic phosphate into cells. Reductions in the blood ionized calcium concentration may be partially responsible for symptoms such as muscle cramps and tetany. Approximately 50% of calcium is bound to albumin, and an increase in pH results in an increase in binding." ... 

Telithromycin may cause clinically significant QTc prolongation and increased risk of ventricular arrhythmia in predisposed patients. It should not be used in patients with prolonged QT syndrome, uncorrected hypokalemia or hypomagnesemia, profound bradycardia, or in patients receiving certain antiarrhythmics (e.g., quinidine, procainamide, amiodarone) or other agents that prolong QTc (e.g., cisapride, pimozide). 

Alderman MH, Filler LB, Ford CE, Probstfield JL, Oparil S, Cushman WC, et al. Clinical significance of incident hypokalemia and hyperkalemia in treated hypertensive patients in the antihypertensive and Hpid-lowering treatment to prevent heart attack trial. Hypertension 2012 59 926-33. 

Tolerance to the diuretic action of caffeine was demonstrated more than 50 years ago and was shown to develop on chronic caffeine intake so that the clinical significance of hypokalemia and calciuria is difficult to evaluate. Although controversial, some epidemiological studies have implicated caffeine in the increased risk for poor calcium retention. For calcium intakes lower than 750 mg per day, increased rate of bone loss and lower bone density were reported. However, it has been suggested that the effect on bone of high caffeine intake requires a genetic predisposition toward osteoporosis. In individuals who ingest calcium recommended daily allowances, there is no evidence of any effect of caffeine on bone status and calcium economy. 

Sodium phosphate is available as a nonprescription liquid formulation and by prescription as a tablet formulation. When taking these agents, it is very important that patients maintain adequate hydration by taking increased oral liquids to compensate for fecal fluid loss. Sodium phosphate frequently causes hyperphosphatemia, hypocalcemia, hypernatremia, and hypokalemia. Although these electrolyte abnormalities are clinically insignificant in most patients, they may lead to cardiac arrhythmias or acute renal failure due to tubular deposition of calcium phosphate (nephrocalcinosis). Sodium phosphate preparations should not be used in patients who are frail or elderly, have renal insufficiency, have significant cardiac disease, or are unable to maintain adequate hydration during bowel preparation. 

Since chronic renal insufficiency is frequently complicated by rises in serum potassium, phosphate, and magnesium, parenteral nutrition solutions used to treat malnourished patients with chronic renal insufficiency are usually prepared with little supplementation of these cations. Four patients with chronic renal insufficiency developed significant hypophosphatemia 3-5 days after starting parenteral nutrition. Other electrolyte abnormalities included hypomagnesaemia (n = 1) and hypokalemia (n — 3) (50). Hypophosphatemia may be the most significant of the electroljde risks in this clinical setting, and the electrolytes of such patients should be monitored closely when nutritional support is begun. 

The clinical manifestations of hypocalcemia are quite variable. The acuteness of the development of hypocalcemia plays a large role in whether or not symptoms will occur." The more acute the drop in ionized calcium concentration, the more likely the patient will develop symptoms. Thus acid-base balance plays a significant role in the hkeiihood of the development of hypocalcemic symptoms, with alkalosis predisposing to symptom development. Concomitant hypomagnesemia, hypokalemia, hyponatremia, and additive side effects from prescribed medications also increase the likelihood of symptomatic presentation. 

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