Earlier in Fluid and Electrolyte disturbances, we talked about Sodium, Hyponatremia, and Hyperkalemia. In this blog, potassium is going to be the target. Potassium is another mineral required in our body in minute amounts, yet it holds significant functions like resting cell membrane potential, hormone secretion, BP, glucose and insulin metabolism, renal concentrating ability, fluid-electrolyte balance, etc.
However, even if this small amount increases, and causes hyperkalemia; if decreases, causes hypokalemia. Therefore, low potassium levels and high potassium levels are still not to be missed.
Normal Value and Physiology
Normal serum potassium concentration ranges between 3.5-5 mEq/L. Homeostasis of potassium balance is maintained through intake and renal excretion. It is mainly regulated by aldosterone.
Aldosterone, diuretics (sodium delivery increased), osmotic diuretics (urine flow increased), high blood potassium levels, glucocorticoids, and ADH (anti-diuretic hormone), all increase the renal excretion of potassium.
Upon increase of potassium levels, an aldosterone-mediated mechanism increases the excretion of potassium via the kidney. Therefore, any factor which increases potassium uptake in cells, thereby increasing potassium levels, will increase its renal excretion via aldosterone.
Enhancers of potassium entry into cells: Insulin, Beta-adrenergic stimuli, and Alkalosis
Factors decreasing potassium entry into cells: Glucagon, Alpha-adrenergic drugs, and Acidosis
Hypokalemia is defined as low serum potassium levels going below 3.5 mEq/L. The mechanism included in hypokalemia are increased losses, decreased intake, or transcellular shift.
Vomiting is a common cause of hypokalemia, which produces volume depletion and metabolic acidosis. On one hand, volume depletion initiates secondary hypoaldosteronism, which increases sodium resorption, therefore increasing potassium excretion.
On other hand, metabolic acidosis also increases potassium excretion as there are fewer hydrogen ions for secretion in response to sodium resorption.
The following table lists the causes of hypokalemia, which include Increased losses of Potassium, Decreased intake or stores of Potassium, and an Intracellular shift of Potassium from intracellular to extracellular.
|Increased losses||Renal loss: RTA (Renal tubular acidosis), Drugs like loop diuretics and thiazides, steroids, cystic fibrosis, Gilet man syndrome, Barter syndrome, Liddle syndrome, mineralocorticoid excess (Cushing syndrome, hyperaldosteronism, congenital adrenal hyperplasia), renin secreting tumors, renal artery stenosis
Extra-renal loss: Diarrhea, vomiting, sweating, potassium binding resins
|Decreased intake or stores||Malnutrition, anorexia nervosa; potassium-poor parenteral control|
|Intracellular shift||Alkalosis, medications like beta-2 adrenergic agonists, theophylline, and barium; refeeding syndrome, hypokalemic periodic paralysis, high insulin state, malignant hyperthermia, and thyrotoxic periodic paralysis.|
Signs and Symptoms
Hypokalemia or low potassium levels causes signs and symptoms which are related to muscular or cardiac functions. Severe hypokalemia, i.e, less than 2.5 mEq/L produces muscle weakness and cardiac arrhythmia.
Low potassium levels are further assessed using a ratio component called TTKG or Trans-tubular potassium gradient. It is calculated as:-
TTKG = (urine potassium x serum osmolality) / (serum potassium x urine osmolality)
If TTKG is less than 4, it means that kidneys are not wasting excessive potassium and the cause is extra-renal. If TTKG is more than 4, it means renal loss is the cause of hypokalemia.
The diagnostic approach to Hypokalemia is made as follows:
Using the diagnostic approach, the underlying cause is found and treated. If TTKG is less than 4, causes of GIT loss, transcellular shift, and poor intake are corrected.
If the TTKG is more than 4, acidosis or alkalosis is explained and corrected. Hypertension associated with metabolic acidosis generally clues toward primary hypoaldosteronism or genetic disease.
Potassium level deficit is corrected over 24 hours, if severe hypokalemia (low potassium less than 2.5 mEq/L) or associated with cardiac arrhythmia, then IV corrections may be necessary.
Hyperkalemia or increased potassium levels is defined as serum potassium levels going above 5.5 mEq/L. The major mechanisms involved are decreased losses, increased intake, extracellular shift, and cellular breakdown.
Renal insufficiency, acidosis, and diseases involving defects in mineralocorticoid, aldosterone, and insulin are some major causes of high potassium levels.
Pseudo-hyperkalemia is caused by thrombocytosis, leukocytosis, and packed red blood cell infusion.
True hyperkalemia is caused by one or more of 3 mechanisms: Increased potassium intake, extracellular potassium shifts, or decreased excretion.
Signs and Symptoms
Sudden and rapid onset of hyperkalemia can result in severe cardiac arrhythmia. Patients often report nausea, vomiting, paresthesias, muscle weakness, fatigue, and ileus.
ECG findings are significant as elevated potassium levels interfere with the repolarization of the cellular membrane during cardiac conduction.
These ECG changes include tall T waves, prolonged PR interval, flat P waves, wide QRS complex, absent P waves, bundle branch blocks, and eventually sine waves.
High potassium levels on sudden and rapid onset are the most serious electrolyte disturbances. They promptly need to be treated. Treatment of hyperkalemia involves discontinuation of potassium-containing fluids and medications which are causing hyperkalemia.
Stabilization of the myocardial cell membrane to prevent cardiac arrhythmia is another important step. Cellular uptake of potassium is enhanced, for which insulin and glucose, sodium bicarbonate, or beta-adrenergic agonists may be used
Diuretics are used to ensure total body potassium elimination only if kidneys are not compromised. Finally, hemodialysis may be required for the treatment of severe symptomatic hyperkalemia that is resistant to drug therapy with patients having impaired renal functions.