HYPERKALEMIA

Dr.Gireesh kumar.K.P
Defenition
• Hyperkalemia is defined as serum potassium greater than
5.5 mEq/L
Cause - Reduced excretion - Most important
• Acute or chronic renal failure – (Most common cause in
clinical practice. If a patient with renal failure come with
bradycardia ,think hyperkalemia)
• Potassium sparing agents – Spironolactone,
• Hypoaldosteronism
• ACE inhibitors (Decreases aldosterone synthesis;
hyperkalemia often can be reduced by concomitant
diuretic use) - ARBs less likely to cause hyperkalemia
than ACE inhibitors
• Trimethoprim and pentamidine
Causes
• Increased intake
• IV Fluids containing potassium
• High potassium containing food or drugs
• Packed red blood cells: Stored cells can partially
• hemolyse and release potassium when infused.
• Tissue breakdown
• Bleeding into body cavities
• Hemolysis
• Rhabdomyolysis
Causes - Shift of potassium out of cells
• Metabolic acidosis: In patients with metabolic acidosis
(lactic acidosis or ketoacidosis) buffering of excess
hydrogen ions in the cells leads to potassium shift into the
ECF.
• Hyperkalemic periodic paralysis
• Beta blocker- Increased beta-2-adrenergic activity drives
potassium into the cells
• Digitalis toxicity- due to dose-dependent inhibition of the
Na-K-ATPase pump
Clinical Features

• Most patients are asymptomatic, symptoms starts at

potassium levels around 6.5 to 7 mEq/L
• Muscular weakness, Hyporeflexia, Progressive ascending
paralysis
• Respiratory muscle weakness – respiratory arrest
• Bradycardia: Bradycardia will be one of the most striking
clinical findings
• Cardiac arrhythmias, cardiac arrest
ECG
Serum K+ levels ECG changes

6 to 7 mEq / L Tall peaked T waves, Short QT interval

7 to 8 mEq / L Loss of P waves, widening of QRS

8 to 10 mEq / L Sine wave (QRS widens and merges with T wave)

> 9 mEq / L Ventricular tachycardia, Atrial fibrillation, cardiac

Arrest
ECG - Tall T waves
Management -Prevention of cardiac arrhythmias
• Calcium directly antagonizes the membrane actions of
hyperkalemia,It decreses membrane excitability, while
hypocalcemia increases the cardiotoxicity of
hyperkalemia
• Injection Calcium Gluconate 10% solution 10 ml (1
ampoule) over 10 minutes.
• Administration of calcium gluconate decreases membrane
excitability.
• The effect begins within minutes but lasts for few minutes
(30–60 min), and the dose can be repeated if any change
in the ECG is seen after 5–10 min.
Shifting of potassium into the cells
• Insulin dextrose infusion
• 25 or 50% 100 ml dextrose with 10 units insulin followed by 5% dextrose at
100 ml / hour ( hyperglycemic patients should not be given glucose – only
insulin should be used )
• To avoid hypoglycemia, subsequent infusion of 5% dextrose at 50 to
75 mL/hour and close monitoring of blood glucose levels is recommended.
• Although dextrose alone will stimulate insulin release from normal pancreatic
beta cells, a more rapid response occurs when exogenous insulin is given as
IV (with glucose to prevent hypoglycemia).
• If effective, the plasma K+ concentration will fall by 0.5–1.5 mEq/L in 15–30
min, and the effect will last for 4 – 6 hours.
Sodium bicarbonate
• Sodium bicarbonate:If there is a severe metabolic acidosis with
hyperkalemia - IV Sodium bicarbonate(use with caution in routine
cases: SB administration should be restricted for cardiac arrest
related to hypokalemia )
• IV sodium bicarbonate 7.5%, 50 to 100 ml (45 to 90 mEq) is given
as a bolus slowly over 10 to 20 minutes followed by IV NaHCO3
drip.In cardiac arrest use Sodium Bicarbonate: 50 mEq IV over 5
minutes
• IV sodium bicarbonate can also shift K+ into cells - Raising the
blood pH with sodium bicarbonate results in hydrogen ion release
from the cells as part of the buffering reaction. This leads in to
potassium movement into the cells to maintain electroneutrality.
• The onset of action is 5 min, and the effect lasts 1-2hours
Salbutamol
• Salbutamol in Nebulized form, it promote cellular uptake
of K+.
• Salbutamol can be given as 10 to 20 mg in 4 mL of saline
by nebulization over 10 minutes (which is 4 to 8 times the
dose used for bronchodilation).
Removal of potassium
• Loop (eg, Furosemide 80 -100 mg IV )or Thiazide
diuretics
• Furosemide has a slow onset of action (1 hour), and its
effect on lowering the potassium level is inconsistent.
Large doses may be needed in renal failure.
• Hemodialysis or peritoneal dialysis ( Peritoneal dialysis
removes K+ is only 15–20% as effective as hemodialysis )
Cation exchange resins
• Cation exchange resins (Oral / Per-rectal /Enema of
Sodium Polystyrene Sulphonate 15 gm TID) which bind
potassium in GI Tract and prevents its absorption. Each
gram binds 1 mEq of K+
• Oral 15-30 gms mixed in water TID
• Enema :50gms in 50 ml of 70% sorbitol mixed in 100 ml
water,retained for 1 hour
• Sodium zirconium cyclosilicate 10 g PO TID for up to 48
hr,then 10 gm OD