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Causes of Hyperkalemia

  1. Renal failure
  2. Decreased K+ secretion
    1. Impaired Na+ reabsorption
      1. Primary hypoaldosteronism: adrenal insufficiency, adrenal enzyme deficiency (21-hydroxylase, 3-hydroxysteroid dehydrogenase, corticosterone methyl oxidase)
      2. Secondary hypoaldosteronism: hyporeninemia
      3. Resistance to aldosterone: pseudohypoaldosteronism.
      4. Drugs (K+-sparing diuretics, trimethoprim, pentamidine), drugs (ACE inhibitors, NSAIDs, heparin)
    2. Enhanced Cl- reabsorption (chloride shunt)
      1. Gordon's syndrome
      2. Cyclosporine

Clinical Features

  1. Malaise, muscle weakness, which may progress to flaccid paralysis and hypoventilation if the respiratory muscles are involved.
  2. Cardiac toxicity: Arrhythmia, palpitation, sudden death
    1. The earliest electrocardiographic changes include peaked T waves.
    2. More severe degrees of hyperkalemia result in a prolonged PR interval and QRS duration.
    3. Atrioventricular conduction delay.
    4. Loss of P waves.
    5. Progressive widening of the QRS complex sine wave pattern.
    6. The terminal event is usually ventricular fibrillation or asystole.

Treatment of Acute hyperkalemia

  1. Severe hyperkalemia requires emergent treatment directed at minimizing membrane depolarization, shifting K+ into cells, and promoting K+ loss.
  2. Administration of calcium gluconate decreases membrane excitability. But it does not reduce S. potassium level.
  3. Insulin with glucose causes K+ to shift into cells. It is the fastest, earliest & the best way to reduce S. potassium level.
  4. When administered parenterally or in nebulized form, 2-adrenergic agonists promote cellular uptake of K+
  5. There is no role of NaHCO3 in the treatment of hyperkalemia (Ref. Hari. 18th ed., pg - 359).

Treatment of Chronic hyperkalemia

  1. Removal of K+ can be achieved using diuretics, cation-exchange resin, or dialysis.

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