Hyperkalemia: protect the myocardium, shift potassium, remove potassium, and recheck. Do these in parallel when severe or accompanied by ECG change. Do not wait for a dramatic ECG because sensitivity is imperfect.
A
Hyperkalemia emergency bundle
verify order set
Purpose
Representative adult action
Clock / caution
Confirm & monitor
Repeat nonhemolyzed potassium when pseudohyperkalemia is plausible, but treat immediately if unstable. ECG + continuous monitor. Glucose/creatinine/bicarbonate
Repeat K at 1, 2, 4, 6 and 24 h after treatment, more often if unstable. A normal ECG does not make severe hyperkalemia safe
Stabilize membrane
For hyperkalemic ECG toxicity, follow an explicit calcium-salt protocol. UKKA: 10% calcium gluconate 30 mL (3 g) over 10 min or 10% calcium chloride 10 mL (1 g) over 5 min
Equivalent elemental calcium (~6.8 mmol), not equivalent grams. Recheck ECG and repeat for persistent toxicity. Chloride is more caustic. Calcium does not lower K
Shift intracellular
Regular insulin 10 units IV + dextrose 25 g under glucose protocol. Add nebulized albuterol 10–20 mg
Glucose at baseline, every 30 min for 2 h, then hourly through at least 6 h after insulin. Extend after repeat insulin or high hypoglycemia risk
Acidosis lane
Sodium bicarbonate when significant metabolic acidemia is contributing and sodium/volume load is acceptable
Not reliable as sole routine shift therapy without acidosis
Remove
Stop K sources. Loop diuretic if producing urine and volume status allows. Potassium binder for selected non-immediate removal. dialysis for refractory/severe disease or kidney failure
Binders are not substitutes for calcium/shift therapy in an unstable patient
Animation paused
Original schematic. Shift therapy buys time. Removal limits rebound. Treat in parallel when needed. Arrows are conceptual, not rates or a sequential waiting rule.
Write a RAASi/MRA reintroduction plan rather than permanent reflex discontinuation after correction.
C
Hypokalemia
replace + stop loss
Situation
Direction
Mild/moderate, oral route
Prefer oral KCl in divided doses. Review diuretic/GI losses and acid–base state
Severe, symptomatic, arrhythmia, no oral route
IV KCl using the approved concentration/rate and monitored-access standard. Central access for higher concentrations/rates
Always
Check and replete magnesium. Assess urine potassium when cause is unclear. Repeat K after replacement and account for ongoing losses
Practice boundary: verify calcium formulation/dose, insulin–dextrose hypoglycemia safeguards, binder selection, dialysis triggers, IV potassium rates, and laboratory recheck clocks.
A
Hyponatremia: first classify
do not skip tonicity
1 · Is it hypotonic?Measured serum osmolality. Recognize hyperglycemic/translocational and isotonic laboratory patterns.
2 · How symptomatic?Seizure, coma, severe confusion, vomiting or respiratory compromise makes this an emergency regardless of the number.
3 · Why retaining water?Urine osmolality + urine Na interpreted with volume status, diuretics, kidney/adrenal/thyroid function, HF/cirrhosis, and fluids.
B
Severe symptomatic hypotonic hyponatremia
small controlled rise
Give a 3% saline bolus using the current treatment standard (for example, 150 mL over 20 min in European guidance), reassess symptoms and sodium after each bolus, and repeat only to the defined endpoint.
Initial goal is usually a 4–6 mmol/L rise sufficient to improve severe symptoms, not immediate normalization.
Ceiling, not target: European guidance limits correction to 10 mmol/L in the first 24 h and 8 mmol/L in each subsequent 24 h. For high osmotic-demyelination risk (Na ≤105, alcohol use, malnutrition, liver disease, hypokalemia), use ≤8 mmol/L in any 24 h and aim lower.
Watch for sudden water diuresis. Check Na frequently during active treatment (every 2 h if urine output rises abruptly). Stop active correction and obtain expert desmopressin ± electrolyte-free-water rescue before the ceiling is exceeded.
C
Common hypotonic phenotypes
treat the mechanism
Phenotype
Typical clues
Direction
Hypovolemic
Loss history, low effective volume. Urine Na varies with renal vs extrarenal loss/diuretic
Restore volume, stop losses. Watch for brisk aquaresis and overcorrection
SIAD-like
Hypotonic, inappropriately concentrated urine, urine Na often elevated, clinically euvolemic
Hypernatremia assess volume, urine output/osmolality, access to water, osmotic diuresis, diabetes insipidus. Stabilize circulation first, then replace free water at a chronicity-appropriate rate with frequent sodium checks.
Torsades / severe Mg deficiency IV magnesium may suppress recurrent torsades even with normal serum Mg. Give an immediate unsynchronized shock for sustained polymorphic VT, and correct K/QT drugs.
Kidney failure reduce repeated Mg dosing and monitor for toxicity.
Practice boundary: verify 3% saline bolus size, correction ceilings, DDAVP clamp/rescue approach, hypernatremia rate targets, and magnesium dosing.
A
Five-step read
same order every time
Validate the sample. VBG often suffices for pH in DKA. Venous PCO₂ is not interchangeable with arterial PCO₂ in compensation formulas, especially in shock. Use ABG when precise ventilation/oxygenation matters and compare chemistry total CO₂.
Acidemia or alkalemia? pH identifies the dominant direction. Near-normal pH can hide a mixed disorder.
Primary process. HCO₃⁻ moves with metabolic processes. PCO₂ moves inversely for respiratory processes.
Expected compensation. A value outside the expected range suggests a second process, after accounting for timing, sample quality and chronicity.
Anion gap and delta. Calculate with the laboratory’s normal range, correct for albumin when useful, and interpret delta ratios cautiously.
B
Compensation card
approximate expectations
Primary disorder
Expected response
Metabolic acidosis
Winter: expected PCO₂ ≈ 1.5 × HCO₃ + 8 ± 2
Metabolic alkalosis
Expected PCO₂ rises about 0.7 mmHg per 1 mmol/L HCO₃ rise (approximate. Severe disorders vary)
Acute respiratory acidosis
HCO₃ rises about 1 per 10-mmHg PCO₂ rise
Chronic respiratory acidosis
HCO₃ rises about 3.5–4 per 10-mmHg PCO₂ rise
Acute respiratory alkalosis
HCO₃ falls about 2 per 10-mmHg PCO₂ fall
Chronic respiratory alkalosis
HCO₃ falls about 4–5 per 10-mmHg PCO₂ fall
C
Gap calculations & causes
interpret in context
AGNa − (Cl + HCO₃). Compare with local normal.
Albumin correction add about 2.5 × (4 − albumin g/dL) to measured AG.
High AG causes lactate, ketoacids, kidney failure, toxic alcohols, salicylate, selected drugs/toxins.
Always pair lactate, ketones, renal function, osmolar/toxin context, glucose, chloride, albumin, and medication history with the calculation.
D
Emergency triggers
treat first
Severe acidemia with shock/arrhythmia/respiratory fatigue. Suspected toxic alcohol or salicylate. DKA. Lactic acidosis from shock. Life-threatening hyperkalemia. Rapidly worsening kidney failure.
Stabilize airway/ventilation and perfusion, stop toxin/cause, and involve critical care, nephrology, toxicology, or endocrinology early. Bicarbonate and dialysis decisions are disease-specific.
Clinical-review boundary: compensation values are bedside approximations. Validate unexpected results, account for chronicity, and use disease-specific treatment pathways.
A
Hypocalcemia
ionized when acute/critical
Step
Direction
Confirm
Use ionized calcium in critical illness, symptoms or abnormal albumin/pH. Alkalemia lowers ionized calcium without necessarily lowering total calcium. Albumin-correction formulas can misclassify acute illness
Emergency
Seizure, tetany/laryngospasm, hypotension or significant QT/arrhythmia → monitored IV calcium. A guideline regimen is 10–20 mL of 10% calcium gluconate in 50–100 mL D5W over 10 min, repeated to symptom relief
Calcium gluconate is less caustic peripherally. Calcium chloride delivers more elemental calcium and needs central/peri-arrest handling. Avoid unreviewed calcium-phosphate co-infusion
B
Magnesium
arrhythmia + refractory K/Ca
Low Mg can sustain hypokalemia/hypocalcemia and raise atrial/ventricular arrhythmia risk.
Torsades IV magnesium may suppress recurrent torsades even if serum Mg is normal. Sustained polymorphic VT needs immediate unsynchronized shock. Remove QT drivers.
Replace orally when stable. IV when severe/symptomatic or oral route is unsuitable.
Kidney failure slows clearance. Repeat doses can cause hyporeflexia, hypotension, bradycardia and respiratory depression.
High Mg stop sources, calcium for cardiotoxicity, fluids/diuresis when appropriate, dialysis for severe toxicity/kidney failure.
Trend reflexes, respiratory status and ECG in severe disease.
C
Phosphate
cause + route
Problem
Clues / response
Low phosphate
Refeeding, alcohol, DKA treatment, respiratory alkalosis, sepsis, antacid/binder, renal wasting, ferric carboxymaltose. Severe disease can impair respiratory/cardiac muscle and blood cells
Replace
Oral for many stable cases. IV only severe/symptomatic or no oral route, using Na/K phosphate selected by potassium and kidney function. Recheck calcium, phosphate, K and renal function. Rapid/excess IV phosphate can cause hypocalcemia
Practice boundary: verify elemental-calcium conversions, infusion rates/access, magnesium dosing by kidney function, phosphate thresholds/formulations, refeeding management, and compatibility.
A
Osmolality card
know your formula
Calculation
Use / caution
Calculated osmolality
2×Na + glucose/18 + BUN/2.8, with measured Na in mmol/L and glucose/BUN in mg/dL. Add ethanol by the laboratory’s convention
Effective osmolality
2×Na + glucose/18. Excludes urea and better represents transcellular tonicity
Osmolal gap
Measured minus calculated. An elevated gap can reflect toxic alcohol, ethanol, propylene glycol, mannitol, ketoacidosis or other solutes
Critical limit
A normal or falling gap does not exclude a late toxic-alcohol presentation because parent alcohol is converted to toxic acids
B
High anion gap + osmolar gap
call poison control
Exposure
Clues
Immediate direction
Methanol
Visual symptoms, abdominal pain, severe AG acidosis. Gap may wane late
Fomepizole promptly when suspicion is high. Give folate and consult toxicology/nephrology. Visual deficits, coma/seizures or persistent severe acidosis can mandate dialysis
Fomepizole and toxicology/nephrology now. Dialysis depends on acidosis/gap, coma/seizures, AKI and antidote/level context. Absent crystals do not exclude poisoning
Propylene glycol
High-dose IV solvent-containing drugs, lactate/osmolar gap, kidney failure
Stop exposure, supportive care, toxicology. Dialysis selected severe cases
Salicylate
Mixed respiratory alkalosis + AG acidosis, tinnitus, tachypnea, fever, altered state. Level can mislead
Alkalinize serum/urine and replete K. If intubation is unavoidable, prevent loss of compensatory hyperventilation. Altered mentation, new oxygen-requiring hypoxemia or failed treatment can justify dialysis irrespective of level
C
Sodium correction guardrails
recalculate frequently
Hyponatremia severe symptoms need controlled 3% boluses. Chronic/high-risk patients need conservative correction ceilings and readiness to halt/re-lower.
Potassium repletion itself can raise serum sodium. Include it in the correction plan.
Hypernatremia correct circulatory collapse first, then free-water deficit and ongoing losses. Chronicity and neurologic status set the rate.
Urine output can change suddenly in DI or after restoring volume. Scheduled sodium checks are essential.
Gap note: “pH/PCO₂/HCO₃ ___. AG (albumin ___) ___. Measured/calc osmolality ___/___, gap ___. Ethanol ___. Ketone/lactate/renal/toxin clues ___. Poison control/toxicology plan ___.”
Practice boundary: verify fomepizole dosing, ethanol correction, salicylate bicarbonate treatment, EXTRIP/dialysis criteria, and poison-center consultation.