HyperK MACHINE Mnemonic
MACHINE is a mnemonic for remembering the causes of hyperkalemia (elevated serum potassium above 5.0 mEq/L). Hyperkalemia is a life-threatening electrolyte imbalance that can cause fatal cardiac dysrhythmias. Recognizing the causes, ECG changes, and treatments for hyperkalemia is heavily tested on the NCLEX because potassium is the most dangerous electrolyte when abnormal.
The Mnemonic
"MACHINE"
Breakdown
Medications
ACE inhibitors, ARBs, potassium-sparing diuretics (spironolactone, triamterene), NSAIDs, and potassium supplements can all cause hyperkalemia. Always review the medication list when potassium is elevated. ACE inhibitors and ARBs reduce aldosterone, decreasing potassium excretion.
Acidosis
Metabolic acidosis causes potassium to shift out of cells into the bloodstream as hydrogen ions move into cells (H+/K+ exchange). For every 0.1 decrease in pH, potassium increases by approximately 0.6 mEq/L. Correcting the acidosis will lower the potassium level.
Cellular Destruction
Any condition that causes massive cell destruction releases intracellular potassium into the bloodstream. Examples include crush injuries, tumor lysis syndrome, hemolysis, rhabdomyolysis, severe burns, and massive blood transfusions. Intracellular potassium concentration is 150 mEq/L compared to 3.5-5.0 mEq/L in the blood.
Hypoaldosteronism
Aldosterone promotes potassium excretion in the kidneys. Conditions that reduce aldosterone (Addison's disease, adrenal insufficiency) impair the kidney's ability to excrete potassium, leading to hyperkalemia. Addison's disease causes both hyperkalemia and hyponatremia.
Intake Excess
Excessive dietary potassium intake or IV potassium administration can cause hyperkalemia, especially in patients with renal impairment. IV potassium must always be diluted and infused slowly (never IV push, which can cause cardiac arrest). Maximum rate is typically 10-20 mEq/hour.
Nephropathy (Renal Failure)
The kidneys are responsible for excreting 80% of the body's potassium. Acute or chronic kidney disease significantly impairs potassium excretion, making hyperkalemia one of the most dangerous complications of renal failure. Monitor potassium closely in all patients with decreased GFR.
Excretion Impaired
Beyond renal failure, anything that impairs potassium excretion contributes to hyperkalemia. This includes dehydration, oliguria, urinary obstruction, and medications that reduce renal potassium secretion. Adequate urine output is essential for maintaining normal potassium levels.
Clinical Relevance
Hyperkalemia above 6.0 mEq/L is a medical emergency. ECG changes progress from peaked T waves to widened QRS to sine wave pattern to cardiac arrest. NCLEX treatment priority: (1) IV calcium gluconate to stabilize cardiac membranes, (2) IV insulin with dextrose to shift potassium into cells, (3) sodium bicarbonate for acidosis, (4) Kayexalate (sodium polystyrene sulfonate) to remove potassium from the body, (5) dialysis for refractory cases.
Study Tips
- ✓Potassium above 6.0 mEq/L = medical emergency. First intervention is IV calcium gluconate to protect the heart.
- ✓Never give IV potassium by push. Always dilute and infuse slowly. Rapid IV potassium causes cardiac arrest.
- ✓Peaked T waves on ECG are the earliest sign of hyperkalemia. Know the ECG progression.
- ✓Insulin drives potassium into cells (give with dextrose to prevent hypoglycemia). This is a temporary measure, not a cure.
FAQs
Common questions about this mnemonic
IV calcium gluconate does not lower the potassium level. Instead, it stabilizes the cardiac cell membranes to protect the heart from the dysrhythmogenic effects of hyperkalemia. It works within minutes and provides a window of safety while other interventions (insulin, Kayexalate, dialysis) are initiated to actually lower the potassium. Think of it as buying time for the heart.
Hyperkalemia causes a predictable progression of ECG changes: peaked (tall, narrow) T waves appear first at K+ above 5.5 mEq/L, followed by prolonged PR interval and flattened P waves at K+ above 6.5 mEq/L, then widened QRS complex at K+ above 7.0 mEq/L, and finally a sine wave pattern progressing to ventricular fibrillation and asystole at K+ above 8.0 mEq/L. The progression can be rapid and fatal.