Prolonged QT, torsades de pointes, digoxin sensitivity
Free interactive simulator
Hypomagnesemia
See the whole patient respond.
Click or hover any value to see why it changed.
Built for pattern recognition
Solid chips are direct physiology. Dashed chips are common clinical pairings — not automatic cause and effect.
Load an imbalance
Pick a direction, then a value.
RelationshipsHypomagnesemia lesson
Interactive lab panel
HypomagnesemiaMove any value
Na⁺SodiumWNL
K⁺PotassiumWNL
Cl⁻ChlorideWNL
Ca²⁺CalciumWNL
Mg²⁺MagnesiumPriority
PO₄³⁻PhosphateWNL
ECFVolume (ECF)WNL
pHpHWNL
Bedside monitor · pattern
Hypomagnesemia
Low magnesium removes a membrane brake and unblocks renal potassium wasting, so potassium and calcium fall with it.
Direct physiologyThreshold falls→Hyperexcitable→QT lengthens→Torsades
Common pairingLow potassiumLow calciumAlcohol use, diuretics, PPIs
ECG responseNormal sinus rhythm
Neuronal excitabilityHyperexcitable
SuppressedBalancedHyper
PerfusionEuvolemic
100%
Extracellular volume at baseline. The dashed line marks euvolemia.
What the nurse would notice
Hypomagnesemia across body systems
Tremor, cramps, tetany, hyperreflexia, Chvostek and Trousseau
Agitation, confusion; seizures when severe
Nausea, anorexia, decreased motility
Teaching model, not a clinical calculator. Patterns show high-yield directional relationships under the stated assumption. Real symptoms, ranges and treatment depend on cause, acuity, comorbidities and local protocols.
Signs & symptoms
Present on this panel. Tap any sign to see which values produce it.
How to think through fluid and electrolytes
Do not memorize eight disconnected lists. Move one value, follow what it changes, and connect the lab pattern to the symptoms you see at the bedside.
Excitable or suppressed?
Low calcium or magnesium removes the brakes: tingling, cramps, hyperreflexia, tetany, seizures. High levels add too much brake: weakness, hyporeflexia, lethargy, respiratory depression.
What can stop the heart?
Potassium and magnesium deserve rhythm attention. In dangerous hyperkalemia, stabilize the myocardium first, then shift potassium into cells, then remove it from the body.
Is circulation failing?
A dramatic lab can distract from volume loss. In DKA and major GI loss, restoring circulating volume comes before the correction students notice first.
Clinical reference points: the teaching patterns and safety framing were checked against the 2024 hyperglycemic-crisis consensus, the UK Kidney Association hyperkalemia guideline and the European hyponatremia guideline.
Why values move together
- Mg²⁺ → K⁺ ↓ 0.4 — Magnesium blocks the ROMK channel in the kidney. When magnesium falls the block comes off, the channel dumps potassium into the urine, and every dose of potassium you give follows it out.
- Mg²⁺ → Ca²⁺ ↓ 0.7 — Magnesium is required to release parathyroid hormone and for bone to answer it. Low magnesium therefore drags calcium down and keeps it there — calcium will not correct until the magnesium does. The effect is one-directional: a high magnesium does not push calcium up.
- Ca²⁺ → PO₄³⁻ ↑ 0.3 — The same seesaw from the other end: parathyroid hormone raises calcium and dumps phosphate into the urine, so the two move opposite each other.
- Ionized Ca²⁺ 4.34 — Total calcium reads normal but alkalosis has bound the ionized fraction to albumin — the patient tingles anyway.
Normal values
The reference bands this tool uses. Switch to Set and mark them from memory.
Na⁺Sodium135–145 mEq/L
K⁺Potassium3.5–5.0 mEq/L
Cl⁻Chloride98–106 mEq/L
Ca²⁺Calcium, total8.5–10.5 mg/dL
Mg²⁺Magnesium1.6–2.6 mg/dL
PO₄³⁻Phosphate3.0–4.5 mg/dL
pHArterial pH7.35–7.45
HCO₃⁻Bicarbonate22–26 mEq/L
PaCO₂Arterial CO₂35–45 mmHg
GluGlucose70–110 mg/dL
Reference ranges vary slightly between laboratories and textbooks. These match the ranges used across NurseSavvy.
The rules the simulator follows
These are the couplings behind the model. Each one is a relationship nursing students are directly tested on, and each is applied in both directions.
| Relationship | Rule of thumb | Why |
|---|---|---|
| pH → potassium | K falls about 0.5 mEq/L per 0.1 rise in pH (metabolic); about half that for a respiratory change | Potassium and hydrogen trade places across the cell membrane. Alkalosis drives potassium in, acidosis drives it out — so an acidotic patient’s "high" potassium may be a depleted total body store. |
| Magnesium → potassium | Low magnesium wastes potassium in the urine | Magnesium blocks the renal ROMK channel. Without it, replacement potassium is excreted as fast as it is given — refractory hypokalemia. |
| Magnesium → calcium | Calcium tracks magnesium down | Magnesium is required to release parathyroid hormone and for bone to answer it, so hypocalcemia will not correct until magnesium does. |
| Calcium ↔ phosphate | Reciprocal — one rises as the other falls | Phosphate binds calcium and shuts down vitamin D activation. Above a calcium-phosphate product of about 55, the salts precipitate into soft tissue and vessels. |
| Albumin → total calcium | Total calcium falls 0.8 mg/dL per 1 g/dL of albumin below 4.0 | Half of serum calcium rides on albumin. A low albumin lowers the total without touching the ionized calcium — a lab artifact, not hypocalcemia. |
| pH → ionized calcium | Ionized calcium falls as pH rises | Alkalosis pushes calcium onto albumin. Total calcium reads normal while the patient tetanizes. |
| Glucose → sodium | Measured sodium falls about 1.6 mEq/L per 100 mg/dL of glucose above normal | Glucose holds water outside the cell and dilutes the sodium. The sodium is not truly low, and it will rise as the glucose is treated. |
| Sodium ↔ water | Sodium rises when free water is lost and falls when free water is retained | Sodium is a concentration. Hypernatremia is a water problem before it is a salt problem, which is why it is treated with water rather than by removing salt. |
| Bicarbonate ↔ chloride | They trade to keep the anion gap constant | Vomiting removes hydrochloric acid, so bicarbonate rises and chloride falls — hypochloremic metabolic alkalosis, and it is chloride-responsive. |
| Bicarbonate → PaCO₂ | Winter’s formula: expected PaCO₂ = 1.5 × HCO₃ + 8 | The lungs compensate for a metabolic acidosis within minutes. Kussmaul respirations are the compensation, not a second problem. |
| PaCO₂ → bicarbonate | HCO₃ rises about 3.5 mEq/L per 10 mmHg of chronic CO₂ retention | Renal compensation takes days, which is how a chronic COPD patient holds a near-normal pH at a CO₂ that would obtund anyone else. |
Where every hypo- and hyper- symptom comes from
There are only two variables behind almost the entire symptom list. Potassium sets the resting membrane potential — how charged the cell sits at rest. Calcium sets the threshold it has to reach to fire, and magnesium is calcium's cofactor at the nerve terminal.
Bring the resting potential and the threshold together and cells fire without being asked. That is hypocalcemia and hypomagnesemia: perioral tingling, twitching, cramping, Trousseau and Chvostek signs, laryngospasm, seizures, brisk reflexes, a long QT and torsades.
Push them apart and cells will not fire at all. That is hypercalcemia and hypermagnesemia: lethargy, constipation, hyporeflexia, and — in magnesium toxicity, in this exact order — absent deep tendon reflexes, then respiratory depression, then cardiac arrest.
Potassium is the exception students get wrong, because it is not linear and because the heart reads it backwards. A low potassium hyperpolarizes skeletal and smooth muscle: flaccid weakness, hyporeflexia, paralytic ileus. The same low potassium makes cardiac repolarization slow and unstable: U waves, ST depression, PVCs, torsades. A potassium above roughly 6 leaves cells depolarized and unable to reset, so a HIGH potassium causes weakness too — while the heart moves through peaked T waves, a widening QRS, a lost P wave and finally a sine wave.
pH belongs in this list even though it is not an ion. Alkalosis pushes calcium onto albumin and potassium into cells, so an alkalotic patient tetanizes with a normal total calcium and drifts toward hypokalemia at the same time.
Questions students ask
What is a fluid and electrolyte simulator?
It is an interactive model of a patient’s chemistry panel. You move one value — potassium, sodium, calcium, magnesium, phosphate, bicarbonate, CO₂, glucose, albumin or extracellular volume — and every related value moves the way a real patient’s would, along with the vital signs, the ECG and the assessment findings. It teaches the relationships between electrolytes, which a static normal-values chart cannot show.
Why does potassium not correct until magnesium is corrected?
Magnesium blocks the ROMK potassium channel in the distal nephron. When magnesium is low that block comes off, the channel dumps potassium into the urine, and every dose of potassium you infuse is excreted almost as fast as it goes in. This is refractory hypokalemia, and the fix is to replace magnesium first — the potassium often rises on its own once it is corrected.
Why does a patient with alkalosis get tetany when the calcium is normal?
About half of serum calcium is bound to albumin and biologically inactive. Alkalosis increases that binding, so the ionized (free) calcium falls while the TOTAL calcium reads normal. The membrane only feels the ionized fraction, so the patient gets perioral tingling, a positive Trousseau sign and carpopedal spasm at a total calcium of 9.0. Treat the alkalosis and order an ionized calcium.
Why is the sodium low in DKA?
It is dilutional, not a true sodium deficit. Glucose is an effective osmole that stays outside the cell, so it pulls water out of cells into the extracellular space and dilutes the sodium by about 1.6 mEq/L for every 100 mg/dL of glucose above normal. A sodium of 128 with a glucose of 620 corrects to roughly 136. Treat the glucose and the sodium normalizes — and expect it to rise as the glucose falls.
How do electrolytes affect membrane excitability?
Potassium sets the resting membrane potential and calcium sets the firing threshold, with magnesium acting as calcium’s cofactor. Low calcium or low magnesium drops the threshold toward the resting potential, so nerves and muscle fire spontaneously: tetany, twitching, Trousseau and Chvostek signs, seizures. High calcium or high magnesium pushes the threshold away: hyporeflexia, lethargy, constipation, and eventually absent reflexes and respiratory depression. Potassium is not linear — low potassium hyperpolarizes the cell (weakness, ileus) while a potassium above about 6 leaves the cell depolarized and unable to reset, which causes weakness too.
Why does hypokalemia cause weakness but make the heart MORE irritable?
Skeletal and smooth muscle read a low potassium as a hyperpolarized membrane that is harder to fire — hence flaccid weakness, hyporeflexia and paralytic ileus. Cardiac tissue instead has slow, unstable repolarization at a low potassium, which produces U waves, ST depression, PVCs and torsades de pointes. Same ion, opposite behaviour, and it is one of the most commonly tested distinctions in the topic.
What do you correct first in a patient with several electrolyte imbalances?
Work in this order. First, anything that is changing the ECG right now — hyperkalemia with peaked T waves gets IV calcium to stabilize the myocardium before anything else. Second, magnesium, because potassium and calcium will not correct until it does. Third, volume, because concentration problems often resolve once perfusion is restored. Then the specific electrolyte, and finally the underlying cause. On the simulator, hang a bag and the verdict tells you whether it was the right one for the panel’s top finding.
Is the simulator free?
Yes, completely — no account, no email and no payment. It runs entirely in your browser. NurseSavvy also has a free Learning Center covering every imbalance in the simulator, and a paid question bank if you want NCLEX practice on top.
Is this a clinical calculator?
No. It is a teaching model. The coupling coefficients reproduce the direction and rough magnitude of the relationships nursing students are tested on, so the picture is right even though the numbers are approximations. Never use it for patient care decisions.
Practise this on real NCLEX questions
The simulator is free forever. When you want to test it, NurseSavvy has 4,600+ NCLEX questions with rationales, unlimited full-length practice tests, and a free Learning Center covering every imbalance here.