This document defines and classifies hyperkalemia based on potassium levels. It discusses the clinical presentation, epidemiology, etiology, and pathophysiology of hyperkalemia. The diagnostic methods and management approaches are also outlined. Hyperkalemia is managed through non-pharmacological treatments like dialysis for severe cases. Pharmacological treatments work to antagonize potassium effects, redistribute potassium into cells, or remove excess potassium from the body using calcium, insulin, beta-agonists, cation exchange resins, and diuretics.
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
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…