Hyperkalemia

HYPERKALEMIA

1. HYPERKALEMIA AMRUTHA JOSE PHARMACY PRACTICE NEHRU COLLEGE

2. DEFINITION It is defined as a serum potassium concentration greater than 5.5mEq/L. The normal serum concentration range for potassium is 3.5-5.0mEq/L .

3. It can be classified according to severity Mild hyperkalemia-5.5 6mEq/L Moderate hyperkalemia-6.1-6.9mEq/L Severe hyperkalemia ->7

4. CLINICAL PRESENTATION OF HYPERKALEMIA GENERAL Related to the effects of excessive k+ on neuromuscular, cardiac & smooth muscle cell function

5. SYMPTOM Frequently asymptomatic however patient may complains of Dyspnea Heart palipitation / strpped heart beats. Nausea or Vomiting Chest pain SIGN ECG changes

6. EPIDEMOLOGY Incidence of hyperkalemia in hospitalised patient has been estimated to be 1.4%-10%. Severe hyperkalemia occurs more commonly in elderly patients with renal insufficiency who receive k+ supplementation .

7. ETIOLOGY Four primary cause of true hyperkalemia Increased potassium intake Decreased potassium excretion Tubular unresponseviness to aldosterone Redistribution of potassium into extracellular space

8. HYPERKALEMIA ASSOCIATED WITH INCREASED POTASSIUM INTAKE Fresh vegetables(tomatoes)&fruits( banana,citrus fruit) Latrogenic cause like overreplacement with K/ Cl and administration of potassium containing medication (K penicillin) to susceptable patients.

9. HYPERKALEMIA ASSOCIATED WITH DECREASED RENAL POTASSIUM EXCRETION More common in ARF and CKD DISAESES: selectivehypoaldosteronism,Addisons desease , adrenal insufficiency DRUGS : ACEIs,Angiotensin receptor blocker,Potassium sparing diuretics & Prostaglandin inhibitors,Trimethoprim-sulfmethoxazole etc

10. TUBULAR UNRESPONSIVENESS TO ALDOSTERONE Actual mechanism not known Certain medical conditions such as sickle cell anemia,systemic lupus erythematosus & amyloidosis can produce defect in tubular K+ secretion,possibly as a result of an alteration in aldosterone binding site.

11. REDISTRIBUTION OF K+ INTO EXTRACELLULAR SPACE ACIDOSIS: Uptake of H+, Efflux of K+ HYPEROSMOLALITY: Hypertonic dextrose,Mannitol , iv immunoglobulins PSEUDOHYPERKALEMIA: Serum K+ concentration may also be falsely elevated in some condition & not reflect the actual invivo k+ concentration .Commonly seen in extravascular hemolysis of RBC

12. PATHOPHYSIOLOGY

13. DIAGNOSTIC METHOD RFT Serum electrolytes including Mg,Ca Urine K & Na Osmolality CBC ECG-Peaked T waves,and QRS widening as well as depression of ST - segment

14. MANAGEMENT NON PHARMACOLOGICAL TRAETMENT End stage renal disease patients who present with severe hyperkalemia or with cardiac manifestation of hyperkalemia , should undergo immediate hemodialysis . Dialysis is the most rapid means of lowering K+ compared to bicarbonate,epinerphrine /insulin plus glucose therapy.

15. PHARMACOLOGICAL TREATMENT Three main approaches to the treatment of hyperkalemia 1. Antagonizing the membrane effect of K+ with Ca 2.Driving extracellular K+ into cells 3.Removing excess potassium from the body.

16. IMMEDIATE ANTAGONISM OF CARDIAC EFFECTS OF HYPERKALEMIA I.V Ca serves to protect the heart Recommended dose is 10ml of 10% Ca gluconate,infused intravenously over 2-3min with cardiac monitoring

17. RAPID REDUCTION IN PLASMA K+ CONCENTRATION BY REDISTRIBUTION INTO CELLS Insulin lowers plasmaq K+ Concentration by shifting K+ into cells β₂ agonist most commonly albuterol are effective but underused agents for the acute management of hyperkalemia . salbutamol nebulisations

18. REMOVAL OF POTASSIUM Use of cation exchange resin ,diuretics and /or hemodialysis CATION EXCHANGE RESINS : Sodium polysterene sulfonate (15-30mg of powder ,almost always given in premade suspension with 33% sorbitol )

19. DIURETICS: Loop and thiazide diuretics SODIUMBICARBONATE : May be given for the treatment of significant metabolic acidosis CONTD …