Pathophysiology
Summary
In the context of electrolyte imbalance, potassium plays a pivotal role. Normal serum potassium levels are maintained between 3.5-5 mEq/L, and deviations above or below this range leads to hyperkalemia or hypokalemia, respectively.
Hypokalemia can be triggered by loop & thiazide diuretics, which increase potassium excretion. Diseases featuring increased mineralocorticoid activity (Conn & Cushing’s syndrome) also cause potassium wasting. Secondary hyperaldosteronism, due to conditions like CHF or cirrhosis, results RAAS activation and consequent potassium excretion. Other factors contributing to hypokalemia include type I & type II RTA, hypomagnesemia, and diarrhea. Drugs like insulin & beta-2 agonists lower serum potassium by stimulating Na/K-ATPases, promoting its intracellular shift. Alkalosis, often triggered by vomiting or hyperventilation, shifts potassium intracellularly, also causing hypokalemia.
Clinical manifestations of hypokalemia range from muscle weakness & decreased deep tendon reflexes to more severe complications like EKG abnormalities (flat/inverted T waves, U waves), ascending paralysis, and cardiac conduction abnormalities.
Hyperkalemia often occurs in the backdrop of chronic kidney disease (CKD), which disrupts potassium excretion. Drugs like ACE inhibitors and potassium-sparing diuretics like spironolactone also inhibit potassium excretion. Hypoaldosteronism, such as in adrenal insufficiency, as well as type 4 RTA can also cause hyperkalemia. In traumatic or pathological conditions like rhabdomyolysis or chemotherapy, extensive cell death can result in a release of intracellular potassium, contributing to hyperkalemia. Acidosis can cause also hyperkalemia—as hydrogen ions enter cells in order to raise blood pH, potassium ions shift to extracellular fluid to maintain electrical neutrality.
Clinical features of hyperkalemia included EKG changes, such as ‘peaked’ T waves early and QRS widening in severe hyperkalemia, as well as life-threatening cardiac arrhythmias like heart block, VF/VT, torsades de pointes, or asystole.
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FAQs
Hypokalemia is characterized by a serum potassium level below 3.5 mEq/L and can be attributed to a variety of conditions and medications. Loop and thiazide diuretics increase sodium delivery to the collecting ducts of the kidneys, which subsequently promotes potassium excretion. Diseases with elevated mineralocorticoid activity, such as primary hyperaldosteronism and Cushing's syndrome, also facilitate potassium excretion. Conditions like congestive heart failure (CHF), cirrhosis, and nephrotic syndrome can induce secondary hyperaldosteronism due to relative hypovolemia, leading to potassium wasting. Other factors like renal tubular acidosis types 1 and 2, hypomagnesemia, and the use of insulin and beta-2 agonists like albuterol can also contribute to hypokalemia by either inhibiting potassium absorption or shifting potassium into cells.
Hypokalemia has a broad spectrum of clinical manifestations that primarily affect the muscular and cardiac systems. In the muscular system, patients may experience muscle weakness, decreased deep tendon reflexes, and in severe cases, ascending paralysis. Cardiac manifestations are evident on electrocardiograms (EKGs) and may include flat or inverted T waves, U waves, and cardiac conduction abnormalities such as supraventricular tachycardia and ventricular fibrillation.
Hyperkalemia is defined by elevated serum potassium levels and can arise from several conditions and medications. Chronic kidney disease (CKD) impairs the kidney's ability to filter and excrete potassium, leading to accumulation. Medications like ACE inhibitors and potassium-sparing diuretics can also reduce potassium excretion. Conditions like hypoaldosteronism, as seen in Addison's disease, limit potassium excretion. Furthermore, extensive cell death from conditions such as rhabdomyolysis or chemotherapy can release intracellular potassium into the bloodstream, causing acute hyperkalemia. Insulin deficiency and beta-2 antagonists inhibit Na/K-ATPases, decreasing potassium uptake. Finally, acid-base imbalances like acidosis can elevate serum potassium by shifting it out of cells.
Hyperkalemia presents with a range of symptoms affecting the muscular and cardiac systems. Patients may experience muscle fatigue, weakness, and in severe cases, paralysis. Cardiac manifestations are particularly concerning and can be identified on an EKG. Initial changes include tall, ‘peaked’ T waves, followed by a widening of the QRS complex. Severe hyperkalemia can lead to life-threatening arrhythmias such as ventricular fibrillation, torsades de pointes, or asystole.
Diuretics can have a significant impact on potassium levels, depending on their mechanism of action. Loop and thiazide diuretics increase sodium delivery to the collecting ducts, promoting Na/K exchange and leading to potassium excretion, resulting in hypokalemia. In contrast, potassium-sparing diuretics like spironolactone and amiloride inhibit potassium excretion, potentially contributing to hyperkalemia.
