A small increase in the extracellular potassium level leads to a great change in the ratio of intracellular (i) to extracellular potassium (o), resulting a decrease in the resting membrane potential (Vm= -61.5 log i/o). Potassium is a main intracellular cation (100-150 mmol/L), and the inward potassium current is responsible for the maintenance of resting membrane potential (Vm). What are the clinical consequences of hyperkalemia on the heart? Hospitalized patients with hyperkalemia have a higher mortality rate than those without hyperkalemia, and it is noted that renal insufficiency significantly contributes to the confounding variables. ![]() Clinical manifestation due to hyperkalemia may be vague (i.e., muscular weakness of a non-specific nature, nausea, vomiting and diarrhea), and hyperkalemia is often revealed in incidental laboratory findings. Specifically, diabetic patients or elderly patients with a decreased glomerular filtration rate need to have their potassium level monitored frequently. Medications can affect the serum potassium level, and patients who have taken angiotensin converting enzyme inhibitors/angiotensin receptor blockers, and/or aldosterone antagonists are susceptible to the risk of hyperkalemia. In such a condition, potassium excretion is largely dependent on the delivery of sodium and aldosterone secretion to collecting tubules as well as colonic mucosa. Ninety percent of potassium is excluded from healthy kidneys, but in patients experiencing end-stage renal disease the potassium excretion from the intestine increases. ![]() The renal adaptive system disrupts the acid-base balance and urinary potassium excretion when the glomerular filtration rate declines to less than 15 ml/min/1.73 m2. The prevalence is 2-3% in the general population but is as high as 40-50% in the elderly population with chronic kidney disease. Chronic kidney disease is the most common cause inducing hyperkalemia. ![]() Hyperkalemia is defined as a serum potassium level greater than 5.5 mmol/L.
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