Typically, the potassium level becomes low because too much is lost from the digestive tract due to vomiting, diarrhea, or excessive laxative use.
Sometimes too much potassium is excreted in urine, usually because of drugs that cause the kidneys to excrete excess sodium, water, and potassium (diuretics).
Certain drugs (such as insulin, albuterol, and terbutaline) cause more potassium to move from blood into cells and can result in hypokalemia. However, these drugs usually cause temporary hypokalemia, unless another condition is also causing potassium to be lost.
Hypokalemia is rarely caused by consuming too little potassium because many foods (such as beans, dark leafy greens, potatoes, fish, and bananas) contain potassium.
Potassium, the most abundant intracellular cation, is essential for the life of an organism. Potassium homeostasis is integral to normal cellular function, particularly of nerve and muscle cells, and is tightly regulated by specific ion-exchange pumps, primarily by cellular, membrane-bound, sodium-potassium adenosine triphosphatase (ATPase) pumps. [3] Potassium is obtained through the diet. Gastrointestinal absorption of potassium is complete, resulting in daily excess intake of approximately 1 mEq/kg/day (60-100 mEq). Of this excess, 90% is excreted through the kidneys, and 10% is excreted through the gut. Potassium homeostasis is maintained predominantly through the regulation of renal excretion; the adrenal gland and pancreas also play significant roles. The most important site of regulation is the renal collecting duct, where aldosterone receptors are present. Potassium excretion is increased by the following factors:
Potassium excretion is decreased by the following factors:
An acute increase in osmolality causes potassium to exit from cells. An acute cell/tissue breakdown releases potassium into extracellular space. Kidneys adapt to acute and chronic alterations in potassium intake. When potassium intake is chronically high, potassium excretion likewise is increased. In the absence of potassium intake, however, obligatory renal losses are 10-15 mEq/day. Thus, chronic losses occur in the absence of any ingested potassium. The kidney maintains a central role in the maintenance of potassium homeostasis, even in the setting of chronic renal failure. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate drops to less than 15-20 mL/min. Additionally, in the presence of renal failure, the proportion of potassium excreted through the gut increases. The colon is the major site of gut regulation of potassium excretion. Therefore, potassium levels can remain relatively normal under stable conditions, even with advanced renal insufficiency. However, as renal function worsens, the kidneys may not be capable of handling an acute potassium load. Potassium is predominantly an intracellular cation; therefore, serum potassium levels can be a very poor indicator of total body stores. Because potassium moves easily across cell membranes, serum potassium levels reflect movement of potassium between intracellular and extracellular fluid compartments, as well as total body potassium homeostasis. Several factors regulate the distribution of potassium between the intracellular and extracellular space, as follows:
Physiologic mechanisms for sensing extracellular potassium concentration are not well understood. Adrenal glomerulosa cells and pancreatic beta cells may play a role in potassium sensing, resulting in alterations in aldosterone and insulin secretion. [4, 5] As the adrenal and pancreatic hormonal systems play important roles in potassium homeostasis, this would not be surprising; however, the molecular mechanisms by which these potassium channels signal changes in hormone secretion and activity have still not been determined. Muscle contains the bulk of body potassium, and the notion that muscle could play a prominent role in the regulation of serum potassium concentration through alterations in sodium pump activity has been promoted for a number of years. Potassium ingestion stimulates the secretion of insulin, which increases the activity of the sodium pump in muscle cells, resulting in an increased uptake of potassium. Studies in a model of potassium deprivation demonstrate that acutely, skeletal muscle develops resistance to insulin-stimulated potassium uptake even in the absence of changes in muscle cell sodium pump expression. However, prolonged potassium deprivation leads to a decrease in muscle cell sodium-pump expression, resulting in decreased muscle uptake of potassium. [6, 7, 8] Thus, there appears to be a well-developed system for sensing potassium by the pancreas and adrenal glands. High potassium states stimulate cellular uptake via insulin-mediated stimulation of sodium-pump activity in muscle and stimulate potassium secretion by the kidney via aldosterone-mediated enhancement of distal renal expression of secretory potassium channels (ROMK). Low potassium states result in insulin resistance, impairing potassium uptake into muscle cells, and cause decreased aldosterone release, lessening renal potassium excretion. This system results in rapid adjustments in immediate potassium disposal and helps to provide long-term potassium homeostasis. Hypokalemia can occur via the following pathogenetic mechanisms:
Although poor intake or an intracellular shift by itself is a distinctly uncommon cause, several causes often are present simultaneously. Increased excretion The most common mechanisms leading to increased renal potassium losses include the following:
Gastrointestinal losses, from diarrhea, vomiting, or nasogastric suctioning, also are common causes of hypokalemia. Vomiting leads to hypokalemia via a complex pathogenesis. Gastric fluid itself contains little potassium, approximately 10 mEq/L. However, vomiting produces volume depletion and metabolic alkalosis, which are accompanied by increased renal potassium excretion. Volume depletion leads to secondary hyperaldosteronism, which in turn leads to enhanced cortical collecting tubule secretion of potassium in response to enhanced sodium reabsorption. Metabolic alkalosis also increases collecting tubule potassium secretion due to the decreased availability of hydrogen ions for secretion in response to sodium reabsorption. Extracellular/intracellular shift Hypokalemia caused by a shift from extracellular to intracellular space often accompanies increased excretion, leading to a potentiation of the hypokalemic effect of excessive loss. Intracellular shifts of potassium often are episodic and frequently are self-limited, as, for example, with acute insulin therapy for hyperglycemia. There is a high prevalence of hypokalemia in patients with severe COVID-19 disease. [9, 10] A definitive cause has not yet been determined and there are likely multiple etiologic factors involved. [11] One leading theory posits that COVID-19 infection is triggered by binding of the spike protein of the virus to angiotensin-converting enzyme 2 (ACE2) resulting in disordered rennin-angiotensin system (RAS) activity, which increases as a result of reduced counteractivity of ACE2. This leads to increased reabsorption of sodium and water, thereby increasing blood pressure and excretion of potassium. [9, 12] Regardless of the cause, hypokalemia produces similar signs and symptoms. Because potassium is overwhelmingly an intracellular cation and a variety of factors can regulate the actual serum potassium concentration, an individual can incur very substantial potassium losses without exhibiting frank hypokalemia. For example, diabetic ketoacidosis results in a significant potassium deficit; however, serum potassium in a patient presenting with diabetic ketoacidosis is rarely low and frequently is frankly elevated. Conversely, hypokalemia does not always reflect a true deficit in total body potassium stores. Acute insulin administration can drive potassium into cells transiently, producing short-lived hypokalemia but not signifying potassium depletion. Cardiovascular complications Hypokalemia has widespread actions in many organ systems that, over time, may result in cardiovascular disease. Cardiovascular complications are clinically the most important harbingers of significant morbidity or mortality from hypokalemia. Although hypokalemia has been implicated in the development of atrial and ventricular arrhythmias, ventricular arrhythmias have received the most attention. Even moderate hypokalemia may inhibit the sodium-potassium pump in myocardial cells, promoting spontaneous early afterdepolarizations that lead to ventricular tachycardia/fibrillation. [13] Increased susceptibility to cardiac arrhythmias is observed with hypokalemia in the following settings:
Low potassium intake has been implicated as a risk factor for the development of hypertension and/or hypertensive end-organ damage. Hypokalemia leads to altered vascular reactivity, likely from the effects of potassium depletion on the expression of adrenergic receptors, angiotensin receptors, and mediators of vascular relaxation. The result is enhanced vasoconstriction and impaired relaxation, which may play a role in the development of diverse clinical sequelae, such as ischemic central nervous system events or rhabdomyolysis. Treatment of hypertension with diuretics without due attention to potassium homeostasis exacerbates the development of end-organ damage by fueling the metabolic abnormalities. These patients are then at higher risk for lethal hypokalemia under stress conditions such as myocardial infarction, septic shock, or diabetic ketoacidosis. Muscular complications Muscle weakness, depression of the deep-tendon reflexes, and even flaccid paralysis can complicate hypokalemia. Rhabdomyolysis can be provoked, especially with vigorous exercise. However, rhabdomyolysis has also been seen as a complication of severe hypokalemia, complicating primary hyperaldosteronism in the absence of exercise. [16] Renal complications Abnormalities of renal function often accompany acute or chronic hypokalemia. These may include nephrogenic diabetes insipidus. They also may include metabolic alkalosis from impaired bicarbonate excretion and enhanced ammoniagenesis, as well as cystic degeneration and interstitial scarring. Gastrointestinal complications Hypokalemia decreases gut motility, which can lead to or exacerbate an ileus. Hypokalemia also is a contributory factor in the development of hepatic encephalopathy in the setting of cirrhosis. Metabolic complications Hypokalemia has a dual effect on glucose regulation by decreasing insulin release and peripheral insulin sensitivity. Clinical evidence suggests that the hypokalemic effect of thiazide is the causative factor in thiazide-associated diabetes mellitus. [17] |
What are signs of hypokalemia?
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