hypokalemic


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hypokalemic

 [hi″po-kah-le´mik]
1. pertaining to or characterized by hypokalemia.
2. an agent that so acts.

hypokalemia

(hi?po-ka-le'me-a) [ hypo- + L. kalium, potash + -emia]
An abnormally low concentration of potassium in the blood (less than 3.5 meq/L). Synonym: hypopotassemia See: hyperkalemiahypokalemic (-le'mik), adjective

Etiology

Causes include deficient potassium intake or excess loss of potassium due to vomiting, diarrhea, or fistulas; metabolic acidosis; diuretic therapy; aldosteronism; excess adrenocortical secretion; renal tubule disease; and alkalosis.

Symptoms

Common manifestations of mild to moderate potassium depletion include muscle aches, fatigue, or mild weakness. As potassium concentrations drop significantly below 3.0 mmol/L, ileus, paralysis, or cardiac conduction and rhythm disturbances may arise. Arrhythmias are particularly likely to affect those patients taking digoxin who become hypokalemic.

Prevention

To prevent hypokalemia, patients taking cardiac glycosides or potassium-wasting diuretics are instructed to include potassium supplements in their medical regimens. Potassium-rich foods (such as oranges, bananas, and tomatoes) are not an adequate source of the potassium that is lost by diuresis.

Treatment

Therapy consists of oral, intravenous, or combined potassium replacement.

CAUTION!

Severely hypokalemic patients may require close electrocardiographic monitoring and frequent assessment of plasma potassium levels.

Patient care

Potassium and other electrolyte levels are monitored frequently during replacement therapy to avoid overcorrection leading to hyperkalemia. Fluid balance is monitored. A physician must be notified if the patient's urine output is less than 600 ml/day because 80% to 90% of potassium is excreted through the kidneys. Cardiac rhythm is monitored, and arrhythmias are reported immediately. Additional care is taken if the patient takes a cardiac glycoside because hypokalemia enhances its action. The patient is assessed for indications of digitalis toxicity (anorexia, nausea, vomiting, blurred vision, arrhythmias). Other signs to watch for include decreased bowel sounds, abdominal distention, and constipation.

Prescribed IV potassium replacement is administered slowly with a volumetric device if the concentration exceeds 40 mEg/L. The rate should not exceed 200-250 mEg/24 hr, and the drug should never be given as a bolus because it may precipitate cardiac arrest. If the patient is prescribed a liquid oral potassium supplement, he or she is advised to dilute it in a full glass of water or fruit juice and to sip it slowly to prevent gastric irritation. Safety measures are implemented for the patient experiencing muscle weakness due to postural hypotension. The importance of taking potassium supplements as prescribed is emphasized, particularly if the patient also is prescribed a diuretic or digitalis preparation. The patient is taught signs of potassium imbalance to report, including weakness and pulse irregularities.

References in periodicals archive ?
Hypokalemic paralysis seen in SS is rare and may sometimes mimic hypokalemic periodic paralysis (HPP).
Hypokalemic paralysis may be due to different conditions, but it may raise the suspicion of PHA in combination with a history of generally mild hypertension.
The clinical presentation of hypokalemic quadriparesis with respiratory failure as the first manifestation of pSS is very atypical.
Hypokalemic patients then receive oral potassium if their potassium level was 2.5-3.0 mmol/L, and intravenous potassium if their level was below 2.5 mmol/L.
Hypokalemic paralysis may precede sicca syndrome from three months to four years in patients with a final diagnosis of pSS [17, 18].
However, PAR might have more potent and different effects than those elicited by AA, due to the presence of two other components, potassium and ribose, the synergic action of which allows the correction of the hypokalemic condition found in cancer cells [20].
Weakness, of sudden or insidious onset, is the most common clinical manifestation, followed by cervical ventroflexion related to hypokalemic polymyopathy, that occurs most commonly with potassium concentrations close to 2.5mmol/L-1 (EGER et al., 1983; MACKAY et al., 1999; ASH et al., 2005; REIMER et al, 2005).
In previous studies, rhabdomyolysis related with copper toxicity and hypokalemic muscle weakness were reported in WD patients with muscle weakness (14, 15).
However, recent research and increased utilization of aldosterone/ plasma renin ratio (ARR) as a method for screening has led to the understanding that majority of patients with PA are not hypokalemic, and the current literature now places the incidence of PA between 5-13 percent (2).
Defective sodium-chloride absorption at this site causes urinary wasting of sodium, chloride, potassium, and magnesium, resulting in hypokalemic metabolic alkalosis with normal or reduced blood pressure [1].
The animal was rehydrated before and after surgery with more of electrolyte solutions like Ringers lactate and Calcium borogluconate as cases usually suffers from hypochloremic, hypokalemic and hypocalcaemic metabolic alkalosis as stated by Peshin et al.
Because it bears tremendous similarity with other causes of hypokalemic periodic paralysis but requires different treatment, it should be strongly considered in any case of hypokalemic paralysis, particularly in patients of Asian descent.