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AMRUTHA JOSE
PHARMACY PRACTICE
NEHRU COLLEGE
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 .
It can be classified according to severity
 Mild hyperkalemia-5.5 6mEq/L
 Moderate hyperkalemia-6.1-6.9mEq/L
 Severe hyperkalemia->7
CLINICAL PRESENTATION OF HYPERKALEMIA
GENERAL
Related to the effects of excessive k+ on
neuromuscular, cardiac & smooth muscle cell function
SYMPTOM
Frequently asymptomatic however patient may
complains of
Dyspnea
Heart palipitation/strpped heart beats.
Nausea or Vomiting
Chest pain
SIGN
ECG changes
EPIDEMOLOGY
o Incidence of hyperkalemia in hospitalised patient
has been estimated to be 1.4%-10%.
o Severe hyperkalemia occurs more commonly in
elderly patients with renal insufficiency who
receive k+ supplementation.
ETIOLOGY
Four primary cause of true hyperkalemia
Increased potassium intake
Decreased potassium excretion
Tubular unresponseviness to aldosterone
Redistribution of potassium into extracellular
space
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.
HYPERKALEMIA ASSOCIATED WITH
DECREASED RENAL POTASSIUM
EXCRETION
o More common in ARF and CKD
o DISAESES: selectivehypoaldosteronism,Addisons
desease, adrenal insufficiency
o DRUGS :ACEIs,Angiotensin receptor blocker,Potassium
sparing diuretics & Prostaglandin
inhibitors,Trimethoprim-sulfmethoxazole etc
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.
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
PATHOPHYSIOLOGY
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
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.
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.
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
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 hyperkalem
salbutamol nebulisations
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)
DIURETICS:
Loop and thiazide diuretics
SODIUMBICARBONATE :
May be given for the treatment of significant
metabolic acidosis
CONTD…
Hyperkalemia
Hyperkalemia
Hyperkalemia

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Hyperkalemia

  • 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 o Incidence of hyperkalemia in hospitalised patient has been estimated to be 1.4%-10%. o 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 o More common in ARF and CKD o DISAESES: selectivehypoaldosteronism,Addisons desease, adrenal insufficiency o 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
  • 13.
  • 14. 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
  • 15.
  • 16. 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.
  • 17. 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.
  • 18. 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
  • 19. 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 hyperkalem salbutamol nebulisations
  • 20. 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)
  • 21. DIURETICS: Loop and thiazide diuretics SODIUMBICARBONATE : May be given for the treatment of significant metabolic acidosis CONTD…