Contraction Alkalosis

Urine chloride decides the treatment - Under 10 mEq/L is chloride-responsive: contraction alkalosis, diuretic therapy, GI acid loss, post-hypercapnic alkalosis, cystic fibrosis, exogenous alkali. Over 20 mEq/L is chloride-resistant: hyperaldosteronism, Bartter and Gitelman syndromes, bicarbonate retention, intracellular hydrogen shift. Chloride-responsive corrects with fluid plus chloride and potassium; chloride-resistant does not, and treatment goes after aldosterone with amiloride or triamterene.

A high bicarbonate means dry - The alkalosis is the fingerprint of the volume that left. In the heart failure patient diuresed hard all week, that elevated bicarbonate is telling you about intravascular volume before you have taken a single blood pressure under anesthesia.

They are compensating by hypoventilating - Metabolic alkalosis raises arterial pCO2 through compensatory hypoventilation. Ventilate to a normal ETCO2 and you strip the compensation and worsen the alkalemia; on emergence they will not resume spontaneous breathing until the CO2 climbs well above the number you usually wait for. Set the ventilator to their baseline, not to a textbook target.

Oxygen unloading is impaired - Alkalosis shifts the oxyhemoglobin dissociation curve left, so hemoglobin holds onto oxygen at the tissue. A saturation that looks reassuring overstates what is actually being delivered, and the net effect described for metabolic alkalosis is tissue hypoxia.

Cardiac consequences - The accompanying hypovolemia and potassium and chloride depletion decrease myocardial contractility and provoke arrhythmias. Expect an exaggerated pressure drop on induction and keep the ECG in view.

Neurologic consequences - Cerebral blood flow falls, and patients can be confused with increased neuromuscular excitability. In an elderly diuresed patient, don't write the preop confusion off as age before you have looked at the bicarbonate and the potassium.

Hypokalemia travels with it - The two sustain each other: low potassium drives hydrogen intracellularly and increases renal hydrogen secretion, while the alkalosis shifts more potassium into the cell. Look for a U wave and a prolonged QT on the 12-lead, replete potassium alongside chloride, and use quantitative train-of-four monitoring - hypokalemia prolongs neuromuscular blockade and interferes with reversal. Confirm a train-of-four ratio of at least 0.9 before extubation (2023 ASA neuromuscular blockade guideline). See the Hypokalemia entry for correction detail.

Fluid choice - Normal saline supplies both the volume and the chloride the kidney needs in order to excrete bicarbonate, which makes this one of the few settings where its chloride load is the point rather than the problem. Add potassium chloride to the repletion; restoring volume without chloride and potassium leaves the alkalosis running.

Fix the cause - As long as the diuresis continues the alkalosis re-forms. In an edematous patient who still needs diuresis, potassium-sparing agents are the way through.

Contraction alkalosis is a metabolic alkalosis produced by subtraction rather than addition. A large volume of sodium-rich, bicarbonate-poor fluid is lost, the extracellular compartment contracts around an essentially unchanged pool of bicarbonate, and serum bicarbonate concentration rises without a single bicarbonate ion having been gained. The usual drivers are loop and thiazide diuretic therapy, cystic fibrosis, and congenital chloride diarrhea.

A healthy kidney dumps excess bicarbonate quickly, so an alkalosis only persists when something blocks that: hypovolemia, a reduced effective arterial blood volume, chloride depletion, hypokalemia, a low glomerular filtration rate, or hyperaldosteronism - and hard diuresis supplies most of that list at once. It is a chloride-responsive alkalosis, urine chloride under 10 mEq/L, which is what makes it correctable with salt, chloride and potassium rather than with a drug.