Hyperkalemia refers to an abnormally high level of potassium (K⁺ > 5.0 mmol/L) in the blood. Potassium is essential for maintaining cellular excitability, nerve conduction, and muscle contraction, particularly in the heart.
Because potassium is so critical, both high and low levels can cause life-threatening arrhythmias.
Causes of Hyperkalemia – MACHINE Mnemonic
The mnemonic MACHINE is widely used to recall the key causes of hyperkalemia:
| Letter | Cause | Explanation |
|---|---|---|
| M | Medications | ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, heparin |
| A | Acidosis | Shifts potassium from cells into plasma (metabolic or respiratory acidosis) |
| C | Cellular destruction | Burns, trauma, rhabdomyolysis, tumor lysis syndrome |
| H | Hypoaldosteronism / Hemolysis | Reduced aldosterone → less K⁺ excretion; RBC breakdown releases K⁺ |
| I | Intake excessive | Excess dietary or supplement potassium (rare unless kidneys impaired) |
| N | Nephrons – Renal failure | Kidneys unable to excrete potassium efficiently |
| E | Excretion impaired | Due to urinary obstruction, drugs, or tubular disorders |
Detailed Breakdown of MACHINE Causes
M – Medications
- ACE inhibitors & ARBs: Reduce aldosterone → less potassium excretion.
- Potassium-sparing diuretics (spironolactone, amiloride): Directly retain K⁺.
- NSAIDs: Reduce renal perfusion → impair potassium clearance.
- Heparin: Suppresses aldosterone synthesis.
- Trimethoprim: Acts like amiloride on renal tubules.
A – Acidosis
- Metabolic acidosis (e.g., diabetic ketoacidosis, renal tubular acidosis): K⁺ shifts out of cells as H⁺ moves in.
- Respiratory acidosis: CO₂ retention increases H⁺ concentration → similar effect.
C – Cellular Destruction
- Burns, trauma: Release intracellular potassium.
- Rhabdomyolysis: Muscle breakdown → massive K⁺ release.
- Tumor lysis syndrome: Chemotherapy-induced cancer cell breakdown.
H – Hypoaldosteronism / Hemolysis
- Addison’s disease: Reduced aldosterone → poor renal K⁺ excretion.
- Hemolysis (intravascular): RBC lysis releases potassium.
I – Intake Excessive
- Rare in healthy people (kidneys excrete extra K⁺).
- Seen in renal failure or with IV potassium supplementation errors.
- Potassium-rich foods: bananas, oranges, coconut water, salt substitutes.
N – Nephrons – Renal Failure
- Acute kidney injury (AKI) or chronic kidney disease (CKD): Impaired potassium clearance.
- Major cause of persistent hyperkalemia.
E – Excretion Impaired
- Obstructive uropathy: Post-renal causes.
- Tubular disorders (e.g., Type 4 renal tubular acidosis).
- Medications interfering with tubular function.
Clinical Features of Hyperkalemia
Often asymptomatic until severe.
Early symptoms:
- Muscle weakness
- Fatigue
- Paresthesias (tingling)
- Flaccid paralysis
- Life-threatening arrhythmias (ventricular fibrillation, asystole)
ECG Changes in Hyperkalemia
- Tall, peaked T waves
- Prolonged PR interval
- Wide QRS complexes
- Loss of P waves
- “Sine wave” pattern in severe cases → impending cardiac arrest
Diagnosis
1. Laboratory Tests
- Serum potassium (>5.0 mmol/L).
- Assess renal function (creatinine, urea).
- Acid-base balance (ABG).
- Hemolysis indicators (LDH, haptoglobin).
- Continuous ECG is critical for patients with suspected severe hyperkalemia.
Management of Hyperkalemia
Immediate (Life-threatening Hyperkalemia)
Stabilize cardiac membranes:
- IV calcium gluconate (protects myocardium, does not lower K⁺).
Shift potassium into cells:
- IV insulin + glucose (drives K⁺ intracellularly).
- Beta-2 agonists (salbutamol inhalation).
- Sodium bicarbonate if acidosis present.
Remove potassium from body:
- Loop diuretics (if renal function intact).
- Cation-exchange resins (patiromer, sodium polystyrene sulfonate).
- Dialysis in severe or refractory cases.
Chronic/Long-term Management
- Dietary potassium restriction.
- Adjust medications contributing to hyperkalemia.
- Regular monitoring in CKD patients.
Complications
- Sudden cardiac death due to arrhythmia.
- Muscle paralysis.
- Exacerbation of kidney disease.
Quick Reference – MACHINE Mnemonic
| Letter | Cause |
|---|---|
| M | Medications (ACE inhibitors, NSAIDs, K⁺-sparing diuretics) |
| A | Acidosis (metabolic & respiratory) |
| C | Cellular destruction (burns, trauma, rhabdomyolysis) |
| H | Hypoaldosteronism / Hemolysis |
| I | Intake excessive |
| N | Nephrons (renal failure) |
| E | Excretion impaired |
FAQs
1. What potassium level is considered dangerous?
Potassium >6.5 mmol/L is life-threatening and requires emergency treatment.
2. What is the most common cause of hyperkalemia?
Chronic kidney disease and medications (ACE inhibitors, potassium-sparing diuretics).
3. Why is calcium gluconate used if it doesn’t lower potassium?
It stabilizes cardiac membranes, preventing arrhythmias while other treatments lower potassium.
4. Can diet alone cause hyperkalemia?
Rarely, unless kidneys are impaired or patient is on potassium-retaining drugs.
5. What is the definitive treatment for refractory hyperkalemia?
Hemodialysis.
