Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0mmol/L (3.5 and 5.0mEq/L) with levels above 5.5mmol/L defined as hyperkalemia.
Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or paresthesia. Hyperkalemia can cause an Heart arrhythmia which can result in cardiac arrest and death.Common causes of hyperkalemia include kidney failure, hypoaldosteronism, and rhabdomyolysis. A number of medications can also cause high blood potassium including mineralocorticoid receptor antagonists (e.g., spironolactone, eplerenone and finerenone) NSAIDs, potassium-sparing diuretics (e.g., amiloride), angiotensin receptor blockers, and angiotensin converting enzyme inhibitors. The severity is divided into mild (5.5 – 5.9mmol/L), moderate (6.0 – 6.5 mmol/L), and severe (> 6.5mmol/L). High levels can be detected on an electrocardiogram (ECG), though the absence of ECG changes does not rule out hyperkalemia. The measurement properties of ECG changes in predicting hyperkalemia are not known. Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.
Initial treatment in those with ECG changes is salts, such as calcium gluconate or calcium chloride. Other medications used to rapidly reduce blood potassium levels include insulin with Glucose, salbutamol, and sodium bicarbonate. Medications that might worsen the condition should be stopped, and a low-potassium diet should be started. Measures to remove potassium from the body include diuretics such as furosemide, potassium-binders such as polystyrene sulfonate (Kayexalate) and sodium zirconium cyclosilicate, and hemodialysis. Hemodialysis is the most effective method.
Hyperkalemia is rare among those who are otherwise healthy. Among those who are hospitalized, rates are between 1% and 2.5%. It is associated with an increased mortality, whether due to hyperkalaemia itself or as a marker of severe illness, especially in those without chronic kidney disease. The word hyperkalemia comes from hyper- 'high' + kalium 'potassium' + -emia 'blood condition'.
Medications that interfere with urinary excretion by inhibiting the renin–angiotensin system are one of the most common causes of hyperkalemia. Examples of medications that can cause hyperkalemia include , angiotensin receptor blockers, non-selective , and calcineurin inhibitor immunosuppressants such as ciclosporin and tacrolimus. For potassium-sparing , such as amiloride and triamterene; both the drugs block epithelial sodium channels (ENaC) in the collecting tubules, thereby preventing potassium excretion into urine. Spironolactone acts by competitively inhibiting the action of aldosterone. NSAIDs such as ibuprofen, naproxen, or Celebrex inhibit prostaglandin synthesis, leading to reduced production of renin and aldosterone, causing potassium retention. The antibiotic trimethoprim and the Antihelminthic pentamidine inhibits potassium excretion, which is similar to mechanism of action by amiloride and triamterene.
Mineralocorticoid (aldosterone) deficiency or resistance can also cause hyperkalemia. Primary adrenal insufficiency are: Addison's disease and congenital adrenal hyperplasia (CAH) (including enzyme deficiencies such as 21α hydroxylase, 17α hydroxylase, 11β hydroxylase, or 3β dehydrogenase).
Insulin deficiency can cause hyperkalemia as the hormone insulin increases the uptake of potassium into the cells. Hyperglycemia can also contribute to hyperkalemia by causing Renal physiology in extracellular fluid, increasing water diffusion out of the cells, and causing potassium to move alongside water out of the cells. The co-existence of insulin deficiency, hyperglycemia, and hyperosmolality is often seen in those affected by diabetic ketoacidosis. Apart from diabetic ketoacidosis, other causes that reduce insulin levels, such as the use of the medication octreotide, and fasting, which can also cause hyperkalemia. Increased tissue breakdown such as rhabdomyolysis, , or any cause of rapid tissue necrosis, including tumor lysis syndrome can cause the release of intracellular potassium into blood, causing hyperkalemia.
Beta2-adrenergic agonists act on beta-2 receptors to drive potassium into the cells. Therefore, can raise potassium levels by blocking beta-2 receptors. However, the rise in potassium levels is not marked unless other co-morbidities are present. Examples of drugs that can raise the serum potassium are non-selective beta-blockers such as propranolol and labetalol. Beta-1 selective blockers such as metoprolol do not increase serum potassium levels.
Exercise can cause a release of potassium into the bloodstream by increasing the number of potassium channels in the cell membrane. The degree of potassium elevation varies with the degree of exercise, which ranges from 0.3 meq/L in light exercise to 2 meq/L in heavy exercise, with or without accompanying ECG changes or lactic acidosis. However, peak potassium levels can be reduced by prior physical conditioning, and potassium levels are usually reversed several minutes after exercise. High levels of adrenaline and Norepinephrine have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors, which, when activated, extracellularly decrease potassium concentration.
Hyperkalemic periodic paralysis is an autosomal dominant clinical condition where there is a mutation in the gene located at 17q23 that regulates the production of protein SCN4A. SCN4A is an important component of in skeletal muscles. During exercise, sodium channels normally open to allow the influx of sodium into the muscle cells for depolarization to occur. But in hyperkalemic periodic paralysis, sodium channels are slow to close after exercise, causing excessive influx of sodium and displacement of potassium out of the cells.
Rare causes of hyperkalemia are discussed as follows. Acute digitalis overdose, such as digoxin toxicity, may cause hyperkalemia through the inhibition of sodium-potassium-ATPase pump. Massive blood transfusion can cause hyperkalemia, especially in infants and patients with low glomerular filtration rate (GFR, a measure of kidney function) due to leakage of potassium out of the red blood cells during storage. Giving succinylcholine to people with conditions such as burns, trauma, infection, prolonged immobilisation can cause hyperkalemia due to widespread activation of acetylcholine receptors rather than a specific group of muscles. Arginine hydrochloride is used to treat refractory metabolic alkalosis. The arginine ions can enter cells and displace potassium out of the cells, causing hyperkalemia. Calcineurin inhibitors such as Ciclosporin, tacrolimus, diazoxide, and minoxidil can cause hyperkalemia. Box jellyfish venom can also cause hyperkalemia.
Potassium is eliminated from the body through the gastrointestinal tract, kidney and . In the kidneys, elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone. In sweat glands, potassium elimination is quite similar to the kidney; its excretion is also controlled by aldosterone.
Regulation of serum potassium is a function of intake, appropriate distribution between intracellular and extracellular compartments, and effective bodily excretion. In healthy individuals, homeostasis is maintained when cellular uptake and kidney excretion naturally counterbalance a patient's dietary intake of potassium.
When kidney function becomes compromised, the ability of the body to effectively regulate serum potassium via the kidney declines. To compensate for this deficit in function, the colon increases its potassium secretion as part of an adaptive response. However, serum potassium remains elevated as the colonic compensating mechanism reaches its limits.
Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated , but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself; instead, it results in accommodation. Above a certain level of potassium, the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction, which can cause ventricular fibrillation and/or Bradycardia.
In the medical history, the presence of known Nephrology, Diabetes, and the use of certain (e.g., potassium-sparing diuretics) are important issues. Electrocardiography (ECG) may be performed to determine if there are ECG changes, tachy- or brady-arrythmias.
The serum potassium concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other , as well as levels of catecholamines, play a major role.
ECG findings are not a reliable finding in hyperkalemia. In a retrospective review, blinded cardiologists documented peaked T-waves in only 3 of 90 ECGs with hyperkalemia. Sensitivity of peaked-Ts for hyperkalemia ranged from 0.18 to 0.52, depending on the criteria for peak-T waves.
High dietary sources include meat, chicken, seafood, such as , Avocado has more potassium than banana 5 May 2011, UPI.com and , fruits such as , oranges and nuts.
Some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. Recent literature questions the validity of this concern.
Loop diuretics (furosemide, bumetanide, torasemide) and thiazide diuretics (e.g., chlortalidone, hydrochlorothiazide, or chlorothiazide) can increase kidney potassium excretion in people with intact kidney function.
Potassium can bind to a number of agents in the gastrointestinal tract. Sodium polystyrene sulfonate (Kayexalate) was approved for this use decades ago, and can be given by mouth or rectally. Sodium polystyrene sulfonate given with sorbitol was uncommonly but convincingly associated with Large intestine necrosis; this combination is no longer used.
Patiromer is taken by mouth and works by binding free potassium ions in the gastrointestinal tract and releasing calcium ions for exchange, thus lowering the amount of potassium available for absorption into the bloodstream and increasing the amount lost via the feces. The net effect is a reduction of potassium levels in the blood serum.
Sodium zirconium cyclosilicate is a medication that binds potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions. Onset of effects occurs in one to six hours. It is taken by mouth.
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