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Management of Hypo and Hyperkalemia.pptx

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Management of Hypo and Hyperkalemia.pptx

  1. 1. Management of Hyperkalemia and Hypokalemia Dr. Tehzeeb Sialvi
  2. 2. Points to cover: › Potassium as an electrolyte › Definitions of Hypo and Hyperkalemia › Causes › Clinical Manifestations › Management
  3. 3. Potassium (K+) › Potassium is an alkaline element in group I of the periodic table. › It is predominantly an intracellular electrolyte; 98% is present in the IC space , while only 2% is present extracellularly. › Normal serum levels of K+ are 3.5-5 mEq/L. › Daily K intake of atleast 90 mmol/L (3510 mg/day) is recommended by WHO.
  4. 4. Functions of K+: • Regulates intracellular osmolality • Helps in contraction of smooth and skeletal muscles • Maintains normal cardiac rhythm
  5. 5. Hypokalemia: › It refers to serum potassium <3.5 mmol/L. Causes: › Redistribution into cells: 1. Alkalosis 2. Hyperinsulinemia 3. Beta-2 agonists & Alpha antagonists
  6. 6. › Gastrointestinal losses: With alkalosis: 1. Vomiting 2. NG aspiration With acidosis: 1. Diarrhea 2. Laxative abuse 3. Villous adenoma of rectum 4. Bowel obstruction / fistula
  7. 7. › Renal losses: 1. Diuretics (loop or thiazide) 2. DKA 3. Hyperaldosteronism 4. Decreased circulatory volume 5. Hypomagnesemia
  8. 8. Clinical Features: › Fatigue › Muscular cramps › Ascending paralysis / Respiratory muscle weakness › Abdominal distension due to paralytic ileus › Hypotension/ Hyporeflexia › Paresthesia › Cardiac arrhythmias (atrial, ventricular ectopic beats)
  9. 9. ›ECG Findings: 1. Flattened T- waves 2. U- wave 3. ST- depression
  10. 10. Treatment: › Treat the underlying disorder. › Oral and/or IV potassium replacement. Calculating K+ Deficit: 0.4 x Body weight (in kgs) x (Normal K+ limit – Serum K+) Maintenance dose: 1 mEq = 1 kg K+ replacement: K+ deficit + Maintenance dose
  11. 11. Hyperkalemia: › It refers to serum potassium >5 mmol/L. Causes: › Decreased excretion: 1. Renal insufficiency 2. Drugs (ACEIs, ARBs, K+ sparing diuretics, NSAIDs) 1. Hypoaldosteronism 2. Type IV Renal Tubular Acidosis
  12. 12. › Redistribution out of cells: 1. Tissue injury (Rhabdomyolysis) 2. Insulin deficiency 3. Drugs (Digoxin, Beta- blockers) 4. Resorption of blood (Hematomas, GI bleed) 5. Hyperosmolarity of ECF
  13. 13. › Spurious: 1. Hemolysis of blood samples 2. Fist clenching during blood draws 3. Thrombocytosis 4. Leucocytosis
  14. 14. Clinical features: › Nausea, vomiting and intestinal colic › Muscular weakness › Flaccid paralysis › Cardiac conduction abnormalities › Cardiac arrhythmias
  15. 15. › ECG Findings: 1. Tall, peaked T- waves 2. Wide QRS complex 3. PR prolongation 4. Loss of P- waves 5. Can progress to V-Fib and cardiac arrest
  16. 16. Treatment: • Urgent treatment is required if:  Acute onset  Severe hyperkalemia (>6.5-7 mmol/L) Step 1: Stabilize cell membrane potential:  IV calcium gluconate  10% of 1o ml solution over 2 minutes
  17. 17. Step 2: Shift K+ into cells:  IV glucose and insulin  Inhaled beta-2 agonist (Salbutamol)  IV sodium bicarbonate (if acidosis present) Step 3: Remove K+ from body:  IV furosemide and normal saline  Ion-exchange resin (sodium polystyrene sulfonate/ Kayexalate) orally or rectally  Dialysis (in renal failure or severe, refractory cases)
  18. 18. Thank you!

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