![]() ![]() Moreover, characteristic ECG changes do not manifest in all patients. This variability is dependent on concomitant factors such as magnesium depletion, digitalis therapy, among others. Although cardiac dysrhythmias or ECG changes are more likely to be associated with moderate to severe hypokalemia, there is a high degree of individual variability and can occur with even mild decreases in serum levels. Hypokalemia can result in a variety of cardiac dysrhythmias. It is characterized by potentially fatal episodes of muscle weakness or paralysis that can affect the respiratory muscles. Periodic paralysis is a rare neuromuscular disorder, which is inherited or acquired, that is caused by an acute transcellular shift of potassium into the cells. Severe hypokalemia can also lead to muscle cramps, rhabdomyolysis, and resultant myoglobinuria. Involvement of GI muscles can cause an ileus with associated symptoms of nausea, vomiting, and abdominal distension. Affected muscles can include the muscles of respiration which can lead to respiratory failure and death. Similar to the weakness associated with hyperkalemia, the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis. Significant muscle weakness occurs at serum potassium levels below 2.5 mmol/L but can occur at higher levels if the onset is acute. Symptoms resolve with correction of the hypokalemia. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. Hence, the physical exam should focus on identifying neurologic manifestations and cardiac dysrhythmias.Ĭlinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L unless there is a precipitous fall or the patient has a process that is potentiated by hypokalemia. Clinical manifestations mainly involve the musculoskeletal and cardiovascular systems. Therefore, questioning should focus on the presence of GI losses (vomiting, diarrhea) and underlying cardiac comorbidities, as well as, a thorough review of medications (insulin, beta agonists, diuretic use). The cause of hypokalemia is evident from the patient’s history. GI losses are a common cause of hypokalemia with severe or chronic diarrhea being the most common extrarenal cause of hypokalemia. Increased delivery of sodium and/or non-absorbable ions (diuretic therapy, magnesium deficiency, genetic syndromes) to the distal nephron can also result in renal potassium wasting. Renal potassium losses are associated with increased mineralocorticoid-receptor stimulation such as occurs with primary hyperreninism and primary aldosteronism. Most cases of hypokalemia result from gastrointestinal (GI) or renal losses. Cellular uptake of potassium is promoted by alkalemia, insulin, beta-adrenergic stimulation, aldosterone and xanthines, such as caffeine. However, reduced intake can be a contributor to hypokalemia in the presence of other causes, such as malnutrition or diuretic therapy. ![]() Decreased potassium intake, in isolation, rarely results in hypokalemia due to the ability of the kidneys to effectively minimize potassium excretion. Hypokalemia can occur as a result of decreased potassium intake, transcellular shifts (increased intracellular uptake) or increased potassium loss (skin, gastrointestinal and renal losses). Potassium homeostasis is maintained through a combination of adjustments in acute cellular shifts between the extracellular and intracellular fluid compartments, renal excretion and, to a lesser extent, gastrointestinal losses. Therefore, plasma or serum levels are not a reliable indicator of total body potassium stores. The fraction of potassium in the extracellular fluid is small. Potassium is predominantly intracellular where it is the most abundant cation and involved in cell regulation and several cellular processes. ![]()
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