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normal ranges

when is it an emergency? why?

normal 3.5 - 5.0 mmol/L

Emergency if plasma [K+] >6.5mmol/L

High potassium levels are cardiotoxic as they inactivate sodium channels.

May cause myocardial hyperexcitability leading to VF





muscle weakness,

Kussmaul breathing if associated metabolic acidosis is present


chest pain


may be asymptomatic


hyperkalemia ECG changes


tall tented T waves, small P waves, wide QRS, ventricular fibrillation

Potassium value 5.5-7.5 mEq/L
- Reversible left anterior fascicular block or
left posterior fascicular block
- Tall, peaked, narrow-based T waves
■ Potassium value >7.5-10.0 mEq/L
- First-degree AV block
- Flattening and widening of P waves, later
disappearance of P waves (sinoventricular
conduction) or sinus arrest
- ST-segment depression
■ Potassium value >10.0 mEq/L
- LBBB,RBBB, markedly widened, diffuse
intraventricular conduction delay
- Ventricular tachycardia or fibrillation,
idioventricular rhythm



causes of hyperkalemia

artefactual causes

  1. oliguric renal failure
  2. K+ sparing diuretics (amiloride)
  3. Rhabdomyolysis
  4. Metabolic acidosis
  5. Excess K6 therapy
  6. Addison's disease
  7. Massive blood transfusion
  8. Burns
  9. Drugs: ACEI, suxamethonium

Artefactual results:

  1. haemolysis (difficult venepuncture, clenched fist)
  2. contamination with potassium EDTA anticoagulant in FBC bottles
  3. thrombocythaemia (K+ leaks out of platelets during clotting)
  4. delayed analysis (leaks out of RBCs)


hyperkalemia treatment


ECG monitor and i.v. access
Protect myocardium

• 10 mL of 10% calcium gluconate i.v. over 5 min
• Effect is temporary but dose can be repeated after 15 min

Drive K+ into cells
• Insulin 10 units + 50 mL of 50% glucose i.v. over 10-15 min followed by regular checks of blood glucose and plasma K+
• Repeat as necessary:
    ○ and/or correction of severe acidosis (pH <6.9) - infuse NaHCO3 (1.26%)
    ○ and/or salbutamol 0.5 mg in 100 mL of 5% glucose over 15 min (rarely used)

Deplete body K+ (to decrease plasma K+ over the next 24 hours)
Polystyrene sulphonate resins:
• 15 g orally up to three times daily with laxatives
• 30 g rectally followed 9 h later by an enema

Haemodialysis or peritoneal dialysis if the above fails.


why is K+ toxic to heart?

High potassium levels are cardiotoxic as they inactivate sodium channels. Divalent cations, e.g. calcium, restore the voltage dependability of the channels. Calcium ions protect the cell membranes from the effects of hyperkalaemia but do not alter the potassium concentration.


what stimulates/inhibits K+ uptake into cells?

drives uptake:
    β-adrenergic stimulation

Uptake is decreased by:
• α-adrenergic stimulation
• acidosis - K+ exchanged for H+ across cell membrane
• cell damage or cell death - resulting in massive K+ release.



when does it need to be treated?

[K+] <2.5mmol/l



hypokalemia and digitalis?

hypokalemia exacerbates digoxin toxicity by increasing binding of digoxin to cardiac cells, potentiating its action, and decreasing its clearance.


signs and symptoms of hypokalemia

Muscle weakness








causes of hypokalemia

• Increased renal excretion
○ Diuretics:
  § Thiazides
  § Loop diuretics
• Increased aldosterone secretion
○ Liver failure
○ Heart failure
○ Nephrotic syndrome
○ Cushing's syndrome
○ Conn's syndrome
○ ACTH-producing tumours

• Exogenous mineralocorticoid
○ Corticosteroids
○ Carbenoxolone
○ Liquorice (potentiates renal actions of cortisol)
• Renal disease
○ Renal tubular acidosis Types 1 and 2
○ Renal tubular damage (diuretic phase)
○ Acute leukaemia
○ Nephrotoxicity Amphotericin
○ Aminoglycosides
○ Cytotoxic drugs
○ Release of urinary tract
○ Obstruction
○ Bartter's syndrome
○ Liddle's syndrome
○ Gitelman's syndrome
• Reduced intake of K+
○ Intravenous fluids without K+
○ Dietary deficiency
• Redistribution into cells
○ β-Adrenergic stimulation
○ Acute myocardial infarction
○ Beta-agonists,
e.g. fenoterol, salbutamol
○ Insulin treatment, e.g. treatment of diabetic ketoacidosis
○ Correction of megaloblastic anaemia, e.g. B12 deficiency
○ Alkalosis
○ Hypokalaemic periodic paralysis
• Gastrointestinal losses (urinary K+ <20 mmol/day)
○ Vomiting
Severe diarrhoea
○ Purgative abuse
○ Villous adenoma
○ Ileostomy or uterosigmoidostomy
○ Fistulae
○ Ileus/intestinal obstruction



hypokalemia ECG changes

■ Prominent U waves
■ ST-segment depression, decreased T-wave
amplitude, may be inverted
■ Increase in amplitude and duration of the P

■ Cardiac arrhythmias and AV block may be digitalis related


  1.         Increased amplitude and width of the P wave
  2.         Prolongation of the PR interval
  3.         T wave flattening and inversion
  4.         ST depression
  5.         Prominent U waves (best seen in the precordial leads)
  6.         Apparent long QT interval due to fusion of the T and U waves (= long QU interval)


ALso to consider in hypokalemia

  1.         Hypokalaemia is often associated with hypomagnesaemia, which increases the risk of malignant ventricular arrhythmias
  2.         Check potassium and magnesium in any patient with an arrhythmia
  3.         Top up the potassium to 4.0-4.5 mmol/l and the magnesium to > 1.0 mmol/l to  stabilise the myocardium and protect against arrhythmias – this is standard practice in most CCUs and ICUs