Defined as serum potassium level less than 3.5 mmol/L.

One of the most common electrolyte disorders found in hospitalized patients, with a reported frequency of 20%.

Urinary potassium loss as a cause of hypokalemia is supported by a ratio of urine potassium to urine creatinine greater than 22 mEq per gram creatinine in a spot urine sample.
Urine in sodium and urine chloride levels may distinguish between vomiting, diuretic or laxative therapy and tubulopathies.
Detected in 2-3% of outpatient encounters.
Unlike hyperkalemia, hypokalemia is uncommon and is usually due to prolong time before specimen processing.

Potassium homeostasis is tightly regulated to maintain serum levels, intracellular potassium, and total body potassium.

Ingested potassium is matched by potassium excretion, most of which occurs via the kidney.
In the kidney, potassium secretion is  couple to sodium reabsorption in the cells of the connecting tubule and cortical collecting duct.
The primary regulators of urinary potassium excretion are sodium delivered to the distal nephron in the adrenal hormone aldosterone, which facilitates sodium potassium exchange.

With Hypokalemia, the sodium chloride cotransporter in the distal convoluted tubule is activated, reducing sodium delivery to the principal cells, and aldosterone is suppressed reducing sodium potassium exchange.

Most patients are asymptomatic and are identified on routine laboratory screening evaluation.

Caused by a variety of disorders with either shift of potassium into cells or waste of potassium from the kidneys or gut.

Inadequate intake of potassium is rarely the sole cause of hypokalemia in patients with normal kidneys.

Hypokalemia is characterized as urinary potassium loss, stool potassium loss, or shift of potassium into cells.
A low potassium diet intake and loss of potassium in perspiration alone are uncommon events to account for hypokalemia.
History should suggest etiologies such as Gastrointestinal losses and medication use.
Thiazide and loop diuretics are common causes of excessive urinary potassium loss.

Hypokalemia may be a result of primary aldosteronism, a manageable cause of urinary potassium loss that is often missed in patients with Hypokalemia and Hypertension.

Acute hypokalemia is due to a transient redistribution of potassium from the extracellular to intracellular space and occurs for hours to days and mainly presents as muscle weakness or paralysis and cardiac arrhythmias.

Persistent hypokalemia results in hyperpolarization of cell membranes and muscle weakness.

Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells.



The presence of hypokalemia makes it more likely that cells will depolarize spontaneously. 

Extremely low potassium levels can lead to rhabdomyolysis, arrhythmias, and respiratory paralysis.

Potassium ion concentrations are a major determinant in the magnitude of the electrochemical potential of cells.



Hypokalemia makes it more likely that cells will depolarize spontaneously, leading to PVCs.

Immediate supplementation should be given at serum levels of less than 3.0 mmol/L because of increased risk of arrhythmia below this level.

Severe hypokalemia less than 3.0 mmol/L between 3.5-5.2% of hospitalized patients.

Severe Hypokalemia can cause palpitations, muscle cramps, muscle weakness, and paralysis.

Even mild serum potassium levels of 2.5-3.4 mEq per liter an asymptomatic process has been associated with increased rates of cardiovascular events and all cause mortality.

Severe hypokalemia associated with potential life-threatening complications including: cardiac arrhythmias paralysis, rhabdomyolysis, and diaphragmatic weakness.

Severe levels (less than 2.4 mmol/M) associated with a mortality rate in hospitalized patients of about 31% compared to a mortality rate of 19.4% for patients with a potassium level of 2.5-2.9 mmol/L.

In patients with even mild to moderate hypokalemia with cardiovascular or chronic kidney disease there is an increase morbidity and mortality up to 50%.

Preoperative hypokalemia as with a higher perioperative mortality in patients undergoing cardiac surgery.

Chronic hypokalemia due to ongoing loss of potassium persts for months-years and contributes to paresthesias, renal insufficiency,renal stones, insulin resistance and glucose intolerance and is associated with increased morbidity and mortality.

The causes of chronic hypokalemia are divided into wasting via the kidneys or extratenal routes.

Most cases associated with potassium-depleting medications.

Present in 17% of patients with acute medical illnesses and is more common among the elderly, women, patients with neoplasm, alcohol abuse and in patients on diuretics (Jensen HL et al).

The majority of cases of chronic hypokalemia or related to excessive potassium losses.

When of sudden onset, transcellular potassium shift, and not total potassium depletion is responsible.

Other causes of hypokalemia include tubulopathies such as Bartter syndrome, surreptitious vomiting or medication use, severe hypomagnesemia, which occurs in approximately 20% of individuals using proton pump inhibitors.

Since 98% total body potassium is intracellular, small changes in its distribution family through significant potassium level changes in the extracellular fluid. Such

The kidneys are able to reduce urinary potassium excretion to less than 20 mmol per day so that hypokalemia due to inadequate intake is uncommon.

About 24% of patients with hypokalemia receive inadequate management during hospitalization.

Many causes of metabolic alkalosis are also associated with hypokalemia.

Hypokalemia maintains metabolic alkalosis by shifting hydrogen ions intracellularly resulting in intracellular acidosis that enhances bicarbonate reabsorption in the collecting duct.

Hypokalemia stimulates the apical H+/K+ ATPase in the collecting duct increasing potassium ion reabsorption and corresponding hydrogen ion secretion.

Hypokalemia stimulates renal ammonia production with generation of bicarbonate.

Hypokalemia impairs chloride ion reabsorption enhancing hydrogen ion secretion, and reduces the glomerular filtration rate impairing renal excretion of the excess bicarbonate.

Several extrarenal causes of chronic hypokalemia, such as vomiting and occasionally diarrhea can induce kaliuresis need to massive bicarbonaturia or existing hypomagnesemia.

Urine potassium excretion rateoften fails to reveal the identity of chronic hypokalemia.

40% of patients with chronic normotensive hypokalemia are ultimately diagnosed with gastrointestinal causes or surreptitious diuretic use.

Patients with gastrointestinal causes or diuretic use accounting for hypokalemia usually are female, have weight loss, lower body mass index, the less potassium supplementation.

More than 50% of patients with G.I. potassium loss also have urine K excretion: uncoupled urine sodium two chloride excretions highly suggest this unique group.

The plasma aldosterone renin ratio (ARR) is elevated in primary hyperaldosteronism because of unregulated aldosterone secretion by one or both adrenal glands causing sodium retention and extra volume expansion and suppression of plasma renin.

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