Acetazolamide

• •Acute mountain sickness prophylaxis and treatment
• •Glaucoma — open-angle and acute angle-closure (adjunct)
• •Pseudotumor cerebri / idiopathic intracranial hypertension
• •Metabolic alkalosis from prolonged diuretic use
• •Refractory CHF (synergy with loop diuretic)

Onset 1–2 h PO, minutes IV. Duration 8–12 h. Renal excretion unchanged.

Mild diuretic — minimal hemodynamic effect at usual doses.

Mild metabolic acidosis → compensatory hyperventilation; basis for AMS efficacy (acclimatization-mimicking).

• !Metabolic acidosis (the mechanism — useful for AMS, problematic in COPD)
• !Paresthesias (tingling fingertips/lips, very common)
• !Hypokalemia
• !Renal stones (alkaline urine + low citrate)
• !Sulfa hypersensitivity (cross-reactive with sulfa antibiotics)
• !Aplastic anemia (rare, idiosyncratic)

• ×Sulfa allergy (relative — most patients tolerate)
• ×Severe hepatic disease (hepatic encephalopathy)
• ×Severe renal failure
• ×Adrenocortical insufficiency
• ×Hyponatremia / hypokalemia uncorrected

• ★AMS PHARMACOLOGIC ANALOG OF ACCLIMATIZATION: induces metabolic acidosis → respiratory drive boost → better high-altitude oxygenation. 125 mg bid starting 24 h before ascent is the validated regimen.
• ★PARESTHESIAS = NORMAL: 'pins and needles' in fingertips and around the mouth is so common it's reassuring — confirms the drug is on board. Counsel patients in advance.
• ★ICP / PSEUDOTUMOR: useful adjunct because it reduces CSF production at the choroid plexus. Less common in modern practice (topiramate often preferred for IIH).
• ★PERIOPERATIVE: chronic acetazolamide users arrive with mild metabolic acidosis. ABG interpretation in these patients should account for that — don't 'fix' a chronic adaptation.

• Furosemide

  Inhibits the Na-K-2Cl cotransporter in the thick ascending loop of Henle. Massive natriuresis + kaliuresis + magnesiuresis. Also a venodilator — drops preload within minutes, before diuresis kicks in.

• Mannitol

  Freely filtered, not reabsorbed. Pulls water from tissues into vascular space (transient ↑intravascular volume) then drives osmotic diuresis. Reduces ICP by drawing water across an intact blood-brain barrier.

• Spironolactone

  Competitive antagonist at the mineralocorticoid receptor in the distal nephron → inhibits aldosterone-mediated Na reabsorption + K secretion. Net effect: mild Na/water loss + K retention + Mg retention. Also a weak androgen-receptor antagonist.

• Bumetanide

  Inhibits the Na-K-2Cl cotransporter in the thick ascending limb → potent diuresis. ~40× more potent than furosemide (1 mg bumetanide ≈ 40 mg furosemide).

Browse all classes: /reference/drugs

• •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
• •Miller's Anesthesia, 9e
• •FDA package insert