Hypokalemia potassium deficiency

Drugs that are also known to decrease potassium levels, such as glucocorticoids and digoxin, should be avoided by anyone taking potassium-depleting diuretics. If they are prescribed, a physician should closely monitor the potassium levels of the patient. Potassium deficiency, or hypokalemia, can cause serious and potentially dangerous side effects (see Harmful side effects section). 

The loss of potassium caused by diuretics is their most intensively debated adverse effect, and the extent and significance of the problem has long been disputed. The effect of diuretics on potassium balance and their chnical consequences have been reviewed extensively (50-52,65,100-102). The risks of diuretic-induced hypokalemia have been greatly exaggerated (50,65,102). A fall in plasma potassium is common, but sound studies have consistently showed that diuretics do not deplete body potassium or cause potassium deficiency during longterm therapy in hypertensive patients (50). 

Horse feeds are usually high in potassium. Potassium deficiency in young horses results in decreased growth rate, reduced appetite and hypokalemia. Orphaned foals gained best growth with 8 g K kg feed DM, but hematological characteristics were optimal at 10 g K kg feed DM (Stowe 1971). 

Potassium is abundant in all animal and plant cells. It is the most common intracellular ion in animal cells. It is therefore widespread in most foodstuffs [8] and potassium deficiency in animals from dietary causes is rare [9] in the absence of disease, malnutrition, or unusual dietary practices [10]. Anorectics [11], alcoholics, and those who consume significant quantities of ion-exchanging clays may show hypokalemia. 

Severe potassium deficiency, which most commonly results from diuretic-induced potassium losses, is characterized by a serum potassium concentration of less than 3.5 mmol/1. The adverse consequences of hypokalemia are cardiac arrhythmias, muscle weakness, and glucose intolerance. Moderate potassium deficiency, which commonly results from an inadequate dietary intake of potassium, occurs without hypokalemia and is characterized by increased blood pressure, increased salt sensitivity, an increased risk of kidney stones, and increased bone turnover. An inadequate intake of dietary potassium may also increase the risk of stroke and perhaps other cardiovascular diseases. 

Potassium is abundant in animal and plant cells (Birch and Pradgeham 1994). Hypokalemia (deficiency) and hyperkalemia (accumulation of K[I]) may both occur. As the normal range of K[I] in plasma is small, and the consequences of hyperkalemia fatal, the method of determination must be precise and accurate to detect lower and higher than normal levels (hypokalemia and hyperkalemia, respectively). The preferred method of determination is PISE. 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Conversely, metabolic alkalosis results in hypokalemia as a result of a net loss of hydrogen ion in the serum. In response, the body releases intracellular hydrogen ion into the serum to increase the acidity of the blood in exchange for extracellular potassium ions. This creates a relative deficiency of serum potassium. Serum potassium falls approximately 0.6 mEq/L for each 0.1 unit rise in blood pH. Similarly, this is frequently termed false hypokalemia because there isn t a true deficiency in total body potassium. 

Patients with a jejunostomy are at risk of hypokalemia as weU, so potassium levels must be monitored closely for supplementation. Other patients at risk for potassium depletion include individuals with long-term sodium depletion, magnesium deficiency, or excessive loss from diarrhea. Metabolic alkalosis, which may occur when a patient becomes dehydrated, accelerates the renal excretion of potassium, as all hydrogen ions are conserved in an attempt to correct the acid-base disorder. As bicarbonate ions are excreted renaUy, potassium is taken with them to maintain osmotic balance. 

Low serum potassium, below 3.4 mEq/L (3.4 mmol/L), may be caused by the use of diuretic medications that result in the excretion of potassium in the urine and by the loss of potassium through diarrhea or excessive sweating. Deficient dietary intake of potassium and magnesium (which causes potassium to move into the cells) could contribute to the development of hypokalemia. 

The nurse is not surprised when the patient is diagnosed with diabetes insipidus (i.e., deficient levels of ADH) and anticipates treatment with ADH supplements and fluid replacement. The nurse will watch closely for fluid retention and possible overload in case the dose exceeds the patient s requirements. The nurse would monitor electrolytes and might anticipate potassium supplements for the hypokalemia. 

Excess of potassium in the body causes hyperkalemia and its deficiency causes hypokalemia. 

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