Metabolic alkalosis — Rapid | Doctor’s Passport

Synopsis

Identify chloride-responsive and chloride-resistant metabolic alkalosis, correct its maintenance factors and detect mixed ventilatory or electrolyte danger.

Metabolic alkalosis is a primary bicarbonate increase; respiratory compensation raises carbon dioxide, but a value outside the expected range reveals an additional respiratory disorder.
Generation and maintenance are separate: vomiting may initiate acid and chloride loss, while low effective volume, chloride depletion, hypokalaemia and reduced GFR prevent renal bicarbonate excretion.
A spot urine chloride obtained before treatment helps divide chloride-responsive disease from continuing diuretic or mineralocorticoid-driven chloride-resistant disease, but timing matters.
Vomiting and nasogastric suction, loop or thiazide diuretics, post-hypercapnic physiology, alkali with renal impairment and mineralocorticoid excess are leading causes.
Alkalemia lowers ionised calcium and promotes intracellular potassium shift, so paraesthesia, cramps, tetany and arrhythmia may occur even when total calcium looks normal.
For true chloride-depletion alkalosis, isotonic sodium chloride and potassium chloride can restore renal bicarbonate excretion, but they may be unsafe in oedematous heart or renal failure.
Correct magnesium and potassium actively because potassium depletion increases renal bicarbonate generation and sustains alkalosis through multiple tubular mechanisms.
Acetazolamide, potassium-sparing therapy, acid infusion or dialysis are specialist options for selected resistant or volume-overloaded cases, not routine first-line answers.

Key red flags

Neuromuscular alkalemia

Perioral tingling, carpopedal spasm, cramps, hyperreflexia, confusion or seizure can result from reduced ionised calcium and altered neuronal excitability.

Arrhythmic combination

Palpitations, syncope, ectopy or QT-related ventricular arrhythmia is more likely with concurrent potassium and magnesium depletion or digoxin treatment.

Mixed ventilatory failure

Drowsiness, hypoxia or a carbon dioxide rise beyond expected compensation indicates superimposed respiratory acidosis and requires urgent respiratory support assessment.

Investigation priorities

Venous or arterial blood gasFirst step

Confirm alkalemia, primary bicarbonate elevation and the adequacy of respiratory compensation.

Management branches

ConfirmDefine primary and mixed alkalosis

Bicarbonate or base excess is high, pH is alkalemic or symptoms suggest altered ionised calcium.

Check pH, bicarbonate and carbon dioxide together, compare with expected compensation and identify an additional respiratory acidosis or alkalosis rather than assuming a single process.
Measure chloride, potassium, magnesium, ionised calcium and renal function, review blood pressure, volume state, ventilation and all gastrointestinal and medicine losses.
Obtain urine chloride before saline or the next diuretic dose when feasible, then classify the likely maintenance mechanism and urgency.

Key medicines

Intravenous 0.9% sodium chloridePrescribe through the NICE five-R fluid framework in staged volumes with reassessment, using the patient’s deficit, pressure, urine output, heart failure and renal function rather than a fixed metabolic-alkalosis total.It is ineffective or harmful in active mineralocorticoid excess and may worsen oedematous heart or kidney failure. Monitor lungs, sodium, chloride, pressure and balance and stop when the physiological endpoint is reached.

Potassium chloride replacementChoose oral or approved ready-diluted intravenous potassium chloride from the current measured deficit, symptoms, renal function and local chart, with repeat potassium before further dosing and monitored infusion for high-risk treatment.Never give intravenous concentrate directly or add it casually to a bag. Check magnesium, renal output and ECG risk; overshoot can occur when vomiting stops, diuretics are withheld or kidney function changes.

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