Elevated blood pH (>7.45) due to a primary increase in bicarbonate (HCO₃⁻).
Severe alkalosis can cause neuromuscular irritability (tetany, seizures) and cardiac arrhythmias. It's also fairly common (≈50% of hospitalized patients have alkalosis). Exams frequently probe the causes (e.g., vomiting vs. hyperaldosteronism) and proper management (distinguishing chloride-responsive vs resistant types).
Often subtle symptoms (e.g., weakness, dizziness, paresthesias); severe cases may have confusion, muscle cramps, or tetany from ↓Ca²⁺, and arrhythmias from electrolyte shifts. Clinical features usually stem from the underlying cause (e.g., vomiting, diuretic use).
Common causes: GI H⁺ loss from prolonged vomiting or NG suction (classic hypochloremic, saline-responsive alkalosis). Also renal losses from diuretics (contraction alkalosis). Excess mineralocorticoid (hyperaldosteronism, Cushing's, etc.) causes saline-resistant alkalosis with hypertension and hypokalemia. Other contributors: severe hypokalemia itself, excess alkali intake (antacids, milk-alkali syndrome), or recovery from hypercapnia.
Lab clues: ↑HCO₃⁻, alkaline urine (once excess HCO₃⁻ spills), often hypokalemia and hypochloremia. Arterial blood gas (ABG) shows high pH and high HCO₃⁻ with compensatory hypoventilation (↑PaCO₂ ~45–55 mmHg).
Confirm metabolic alkalosis on ABG: pH >7.45 with high HCO₃⁻ (and elevated PaCO₂ compensating). Calculate expected respiratory compensation: PaCO₂ ≈ 0.7*(HCO₃⁻ − 24) + 40 (±2) mmHg; if actual PaCO₂ is much lower or higher, suspect a mixed disorder.
Check urine chloride to classify: < 20 mEq/L indicates chloride-responsive alkalosis (body Cl⁻ depleted) – typically due to vomiting, NG suction, or remote diuretic use. > 20 mEq/L suggests chloride-resistant alkalosis (kidneys not chloride-conserving) – seen in active diuretic use or mineralocorticoid excess.
If urine Cl⁻ is low: patient likely volume depleted (orthostatic hypotension, dry mucous membranes). If urine Cl⁻ is high: assess volume/BP – hypertension points to hyperaldosteronism or Cushing's; normal or low BP may indicate current diuretic therapy or rare syndromes (Bartter, Gitelman).
Identify the cause and address it: review medication history (diuretics), intake (antacids), and endocrine evaluation (aldosterone/renin levels if indicated). Remember that vomiting causes H⁺/Cl⁻ loss and volume contraction (contraction alkalosis), whereas hyperaldosteronism causes renal H⁺ and K⁺ loss (via excess aldosterone effect).
e.g., in COPD: chronically high PaCO₂ causes elevated HCO₃⁻, but pH is normal/slightly low (not frankly alkalotic); context of longstanding hypercapnia.
For chloride-responsive alkalosis (e.g., vomiting, diuretics): give IV normal saline to correct volume/Cl⁻ depletion and KCl to restore potassium. This allows kidneys to excrete bicarbonate and fix the alkalosis. Treat the underlying cause (antiemetics for vomiting, adjust diuretics, etc.).
For chloride-resistant alkalosis (e.g., hyperaldosteronism): address the source of mineralocorticoid excess. Options include aldosterone antagonists (e.g., spironolactone) or surgical removal of an adrenal tumor. Correct hypokalemia with K⁺ supplementation. If due to excessive alkali intake (milk-alkali), stop the offending agent.
In severe or refractory cases (pH >7.55) not responding to above measures: consider acetazolamide (carbonic anhydrase inhibitor) to enhance HCO₃⁻ excretion. In life-threatening alkalosis (pH >7.60) or renal failure, IV acid (HCl) infusion or dialysis may be used.
Urine Cl⁻ is the key diagnostic clue: <20 = vomiting/diuretics (saline-responsive); >20 = hyperaldosteronism or ongoing diuretics (saline-resistant).
Metabolic alkalosis often comes with hypokalemia (H⁺ shifts into cells, plus RAAS activation causes K⁺ loss) – always check and replete K⁺.
Severe alkalemia (pH >7.60) can precipitate seizures and ventricular arrhythmias – requires urgent intervention (ICU care, possible IV acid or dialysis).
Metabolic alkalosis + hypertension + hypokalemia → suspect primary hyperaldosteronism (Conn syndrome) – a treatable endocrine cause often missed if focusing only on volume status.
Identify alkalosis: pH >7.45 on ABG → check HCO₃⁻. If HCO₃⁻ is high (with elevated PaCO₂), primary metabolic alkalosis is present.
Evaluate compensation: expected PaCO₂ ≈ 0.7*(HCO₃⁻ − 24) + 40 mmHg. If actual PaCO₂ deviates beyond ±2 mmHg, there is a mixed disorder.
Measure urine Cl⁻: if <20 mEq/L → chloride-responsive alkalosis (likely GI losses or past diuretic use); if >20 mEq/L → chloride-resistant alkalosis or current diuretic use.
If Cl-responsive (low urine Cl⁻): patient is volume contracted – treat with IV saline + KCl, and fix the cause (e.g., antiemetics for vomiting).
If Cl-resistant (high urine Cl⁻): check BP and edema. If hypertensive or hypervolemic → investigate hyperaldosteronism or Cushing's (endocrine causes). If normotensive → consider active diuretics or rare tubulopathies (Bartter/Gitelman). Manage accordingly (halt diuretics, treat endocrine cause).
Young woman with an eating disorder (bulimia) who has frequent vomiting, paresthesias, and lab showing ↑HCO₃⁻/↑pH/low Cl⁻ → metabolic alkalosis from vomiting (saline-responsive).
Patient on high-dose loop diuretics (e.g., for hypertension or heart failure) with weakness and contraction signs → metabolic alkalosis due to diuretic use (volume contraction alkalosis).
Hypertensive patient with muscle weakness, hypokalemia, and metabolic alkalosis → primary hyperaldosteronism (excess aldosterone causing H⁺/K⁺ loss).
Case 1
A 24‑year‑old woman with a history of bulimia nervosa presents with dizziness and muscle cramps.
Davenport diagram illustrating acid-base balance; metabolic alkalosis resides in the high pH, high HCO₃⁻ quadrant.
