Metabolic Alkalosis (Study Outline) 1. Background Definiti…
Metabolic Alkalosis (Study Outline) 1. Background Definition: A primary increase in serum HCO₃⁻ leading to elevated blood pH (>7.45), with compensatory hypoventilation (↑ PaCO₂). Pathophysiology: Requires generation of excess bicarbonate and maintenance due to impaired kidney excretion of HCO₃⁻. Frequently associated with volume depletion, RAAS activation, and hypokalemia, which promote HCO₃⁻ retention. Major etiologic categories: Chloride-responsive (volume-depleted): Vomiting, NG suction (loss of gastric acid). Diuretics. Post-hypercapnia correction. Chloride-resistant (volume-expanded): Hyperaldosteronism (primary or secondary). Cushing syndrome. Severe hypokalemia. High-yield concept: Urine chloride helps differentiate causes. 2. History GI losses: nausea, vomiting, recent NG tube suction. Diuretic use: loop/thiazide history. Endocrine symptoms: hypertension, muscle weakness, polyuria (aldosteronism). Neuromuscular symptoms: paresthesias, cramps, tetany (due to associated hypocalcemia). Hypovolemia symptoms: dizziness, thirst, orthostatic lightheadedness. 3. Exam Findings Vitals: may show hypotension (volume depletion) or hypertension (hyperaldosteronism). Signs of hypovolemia: dry mucous membranes, tachycardia, orthostasis. Neurologic: Chvostek/Trousseau signs (alkalosis increases protein-bound Ca²⁺). Cardiac: arrhythmias from hypokalemia. Physical clues to etiology: Abdominal distension/tenderness (vomiting). Cushingoid features (if steroid excess). 4. Making the Diagnosis ABG/BMP: High pH, high HCO₃⁻, compensatory ↑ PaCO₂ (but rarely >60 mm Hg). Serum electrolytes: Low Cl⁻, low K⁺, possibly ↑ aldosterone (if endocrine cause). Urine chloride (high-yield differentiator): 20 mEq/L → Chloride-resistant (hyperaldosteronism, mineralocorticoid excess). Identify precipitating cause: History of vomiting, diuretics, endocrine disease. Gold Standard: ABG + metabolic panel confirming elevated pH and HCO₃⁻, with urine chloride guiding etiology. 5. Management (Exam Concepts) General principles: Correct underlying cause conceptually (GI losses, diuretic effect, endocrine disease). Avoid nephrotoxins; adjust renal dosing. Chloride-responsive alkalosis: Conceptual volume repletion with chloride to allow renal excretion of HCO₃⁻. Address vomiting/NG losses at conceptual level. Chloride-resistant alkalosis: Treat underlying mineralocorticoid excess conceptually. BP control principles. Electrolyte monitoring: Correct hypokalemia and hypochloremia (key for resolving alkalosis). Severe alkalemia: Consider acidifying therapy conceptually in life-threatening cases (exam-level only). Referral: when metabolic alkalosis is severe, recurrent, or linked to endocrine disease. QUESTION A 28-year-old man presents with dizziness, lightheadedness, and persistent nausea. He reports vomiting multiple times daily for the past 4 days due to a viral illness. He denies diarrhea, recent medications, or alcohol use. On examination, he appears dehydrated with dry mucous membranes and orthostatic hypotension. Laboratory results show: Arterial pH: 7.48 HCO₃⁻: 34 mEq/L PaCO₂: 48 mm Hg K⁺: 3.0 mEq/L Cl⁻: 86 mEq/L What is the most appropriate next step in evaluating the cause of his acid-base disorder? A) Measure serum aldosteroneB) Check urine chlorideC) Begin IV saline and potassium chlorideD) Discontinue furosemide therapy