Pathology - Hyperkalemia
Pathophysiology Normal serum potassium levels range from 3.5 to 5.0 mEq/L. Heart arrhythmia is one way that elevated serum potassium depolarizes the resting membrane potential. Hyperkalemia can cause the T-wave on an ECG to become more sensitive; this can lead to initial T-wave peaking and widening of the QRS complex, which can indicate an increased risk of catastrophic ventricular arrhythmias. Intravenous calcium administration rapidly reduces membrane excitability. The serum potassium content can then be brought back to normal by using insulin or beta-adrenergic agonists to induce a potassium shift into the cells. These are only temporary solutions; diuretics or other more effective measures are also required to eliminate excess potassium. In this instance, the renin-angiotensin-aldosterone pathway was disrupted in the context of impaired renal function, which is typical of diabetes, leading to the development of hyperkalemia. Although cellular potassium changes (such as tumor lysis or rhabdomyolysis) can produce hyperkalemia in an acute manner, acute or chronic renal insufficiency is typically linked to the inability to eliminate potassium in the urine to an acceptable degree. Through the promotion of collecting duct secretion, aldosterone is the primary regulator of renal potassium excretion. Thus, hyperkalemia may also result from any disruption of the renin-angiotensin-aldosterone-renal main cell pathway.
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