Clinical Mnemonics · Pharmacology & Electrolytes
MURDER
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In 30 seconds
Lists the body-system effects of hyperkalemia (high blood potassium) — Muscle, Urine, Respiratory, Decreased cardiac contractility, ECG, Reflexes — so the clinician recognizes the patient before the heart stops.
The college version
Status: current, with caveats. The source library flags this one as still taught but qualified — read the safety notes on each component before relying on it.
Lists the body-system effects of hyperkalemia (high blood potassium) — Muscle, Urine, Respiratory, Decreased cardiac contractility, ECG, Reflexes — so the clinician recognizes the patient before the heart stops.
M — Muscle abnormalities
Weakness, cramps, fasciculations, flaccid paralysis
Hyperkalemia partially depolarizes the resting membrane; muscles are first irritable (paresthesias, cramps, fasciculations) then profoundly weak, with an ascending pattern that can become flaccid paralysis and mimic Guillain-Barré.
Physiology. Elevated extracellular K+ makes the resting membrane potential less negative; sodium channels become inactivated, so action potentials can no longer fire normally.
Safety. New ascending weakness in an at-risk patient is a red flag — check ECG and potassium immediately.
U — Urine abnormalities
Oliguria / anuria (the underlying cause)
Impaired renal excretion (AKI or ESRD) is the most common cause of clinically significant hyperkalemia, producing oliguria (<400 mL/day) or anuria (<100 mL/day).
Physiology. The kidneys normally excrete ~90% of daily potassium load; when filtration or tubular secretion fails, serum potassium climbs.
Safety. Weakness of the mnemonic: 'U' is an etiology clue (why potassium is high), not a manifestation of the high potassium itself.
R — Respiratory effects
Hypoventilation → respiratory failure
Progressive weakness of the diaphragm and intercostal muscles causes hypoventilation, CO2 retention, and ultimately respiratory failure — a late, life-threatening manifestation.
Physiology. The diaphragm is skeletal muscle and suffers the same depolarization blockade described under 'M'.
Safety. Monitor respiratory rate, depth, and work of breathing; anticipate possible assisted ventilation.
D — Decreased cardiac contractility
Weak heart squeeze, hypotension
Hyperkalemia depresses myocardial contractility and conduction, producing hypotension and decreased cardiac output that compound the arrhythmia risk.
Physiology. Partial depolarization reduces the force of contraction and slows impulse conduction, causing bradyarrhythmias and heart block.
Safety. Hypotension plus ECG changes is a medical emergency.
E — ECG changes
Peaked T waves → PR/QRS changes → sine wave
Progression: peaked 'tent' T waves (~5.5–6.5 mEq/L), PR prolongation and P-wave loss (~6.5–7.0), QRS widening (~7.0–8.0), then sine-wave pattern → VF/asystole (>8.0).
Physiology. Depolarization slows atrial and ventricular conduction (P-wave loss, PR and QRS prolongation) while repolarization changes produce the peaked T wave.
Safety. ECG does not always correlate with the serum number — treat the patient and ECG, not just the lab value; hyperkalemia can mimic wide-complex VT.
R — Reflex changes
Diminished / absent deep tendon reflexes
Deep tendon reflexes become diminished and then absent as muscle weakness progresses — a late finding paralleling the severity of muscle involvement.
Physiology. Depolarization blockade reduces the muscle's ability to contract in response to the reflex arc.
Safety. Weakness of the mnemonic: reflex changes are nonspecific, late, and easy to miss — rely on ECG and the potassium level for early detection.
Memory aids
- M = Muscle abnormalities
- U = Urine abnormalities
- R = Respiratory effects
- D = Decreased cardiac contractility
- E = ECG changes
- R = Reflex changes
Quick review
- M = Muscle abnormalities — Weakness, cramps, fasciculations, flaccid paralysis
- U = Urine abnormalities — Oliguria / anuria (the underlying cause)
- R = Respiratory effects — Hypoventilation → respiratory failure
- D = Decreased cardiac contractility — Weak heart squeeze, hypotension
- E = ECG changes — Peaked T waves → PR/QRS changes → sine wave
- R = Reflex changes — Diminished / absent deep tendon reflexes
Eli explains
The same idea, in plain words
Explain it like I’m 10
A checklist of the ways too much potassium can hurt the body — from weak muscles and weak breathing to a heart that can't keep its rhythm.
M — Muscle abnormalities. Potassium is the battery that lets muscles fire. Too much drains the battery, so muscles get weak and floppy instead of strong.
U — Urine abnormalities. The kidneys are the drains that flush out extra potassium. If the drains are clogged, potassium backs up in the blood.
R — Respiratory effects. Breathing uses big muscles. If potassium makes muscles weak, the breathing pump gets weak too, and the patient can't move enough air.
D — Decreased cardiac contractility. The heart is a muscle too. Too much potassium weakens its squeeze, like a pump losing power, so blood pressure drops.
E — ECG changes. The ECG photographs the heart's electrical heartbeat; high potassium changes the photo in a predictable order until the rhythm melts into a dangerous squiggle.
R — Reflex changes. When the doctor taps the knee, the leg should kick. If the muscles are too weak, the kick is small or missing.
Study tools & related lessonsKey vocabulary · Related
Key vocabulary
- M
- Muscle abnormalities
- U
- Urine abnormalities
- R
- Respiratory effects
- D
- Decreased cardiac contractility
- E
- ECG changes
- R
- Reflex changes
Sources & references
This lesson was adapted from the open educational references above; their licenses and attributions are preserved. See Copyright & Licensing.
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