Metabolic Alkalosis

Ventilation - Compensation is hypoventilation, and it is limited because CO2 is the drive for respiration. Expect pCO2 = 0.7 x [HCO3] + 21, or roughly a 0.5 to 0.75 mmHg rise for every 1 mEq/L rise in bicarbonate. Once bicarbonate reaches the mid-30s the hypoventilation contributes to failed weaning. On the ventilator, do not drive the pCO2 to 40 - you will stack a respiratory alkalosis on top of the metabolic one.

Left-shifted oxyhemoglobin curve - Alkalemia raises hemoglobin's affinity for oxygen and impairs release at the tissue, and it also accelerates glycolysis, raising tissue oxygen demand. The net effect is tissue hypoxia behind a reassuring SpO2.

Ionized calcium falls - Alkalosis increases calcium binding to albumin, so the ionized fraction drops: reduced contractility, increased neuromuscular excitability, tremor, tingling, carpopedal spasm. Follow ionized calcium rather than total calcium, and remember that the ventilator setting moves that number.

Potassium and magnesium - Hypokalemia both causes and accompanies metabolic alkalosis, and the atrial and ventricular tachyarrhythmias, weakness, and twitching come mostly from the electrolytes rather than the pH itself. Replacing potassium accomplishes nothing if magnesium is also low - replace both.

Urine chloride splits the differential - Under 15 mEq/L is chloride responsive: gastric acid loss from vomiting or NG suction, diuretics, volume depletion, post-hypercapnia, cystic fibrosis, exogenous alkali. Over 25 mEq/L is chloride resistant: mineralocorticoid excess, potassium depletion, Bartter, Gitelman. Chloride-responsive patients are usually volume depleted; chloride-resistant patients are usually volume expanded and hypertensive.

Repletion needs chloride, not just volume - Contraction alkalosis does not correct with volume unless the chloride comes with it, so give 0.9% NaCl. Chloride deficit = 0.2 x weight x (100 - [Cl]); divide that by 154 for the liters of normal saline. KCl is a poor chloride vehicle because it cannot run faster than 40 mEq/h, and it is indicated only when the patient is hypokalemic.

HCl only for a pH above 7.5 - Hydrogen deficit = 0.5 x weight x (measured [HCO3] minus a target of 35), infused at 0.2 mEq/kg/hr and never stronger than 0.1N. It extravasates and causes tissue necrosis even through a central line. Do not use ammonium chloride, which causes encephalopathy in renal or hepatic impairment, or arginine hydrochloride, which causes severe hyperkalemia.

Acetazolamide, with one hard exception - 5 to 10 mg/kg IV or PO for chloride-resistant alkalosis; it blocks bicarbonate reabsorption and diureses, so watch potassium closely. Never give it to a neurosurgical patient - it raises cerebral blood flow and ICP.

Post-hypercapnic alkalosis - Normalize a chronic CO2 retainer's pCO2 on the ventilator and the renally retained bicarbonate lags behind, leaving an alkalosis that self-corrects over days. Ventilate to the patient's baseline pCO2, not to 40.

Massive transfusion - Citrate in banked blood is metabolized to bicarbonate, though it takes roughly 8 units before bicarbonate rises. The same citrate load chelates calcium, so the ionized calcium hit compounds the one the alkalosis is already causing.

Pyloric stenosis - A two to six week old with projectile, non-bilious vomiting and a hypochloremic, hypokalemic alkalosis. The electrolyte derangement, not the pylorus, is what deteriorates the infant - correct chloride, potassium, and volume with saline before induction.

It is not a benign lab value - Metabolic alkalosis tracks with longer ICU stay, more ventilator days, and higher hospital mortality independent of cause; each 5 mEq/L of bicarbonate above 30 mEq/L carries an odds ratio of 1.21 for hospital mortality.

Neurologic effects - Confusion through to coma, decreased cerebral blood flow, and increased neuromuscular excitability. Seizures and carpopedal spasm are more typical of respiratory alkalosis, but a confused post-op patient with a bicarbonate in the 40s deserves a gas before a head CT.

Metabolic alkalosis is a pH above 7.45 with an elevated bicarbonate, and it is the most common acid-base derangement in hospitalized patients at about 51%. It arises from an intracellular hydrogen shift (hypokalemia), gastrointestinal hydrogen loss (vomiting, NG suction), renal hydrogen loss (mineralocorticoid excess, loop and thiazide diuretics, Bartter and Gitelman syndromes), added or retained bicarbonate (sodium bicarbonate, milk-alkali syndrome, citrate in banked blood, post-hypercapnia), or contraction around a fixed bicarbonate pool.

A working kidney dumps excess bicarbonate quickly, so alkalosis only persists when something blocks that: hypovolemia, chloride depletion, hypokalemia, a low GFR, or hyperaldosteronism. That is the useful part at the board - the alkalosis is a symptom of the block, and it corrects when you correct the block.