A 41-year-old man with Child-Pugh Class C cirrhosis presents to the emergency department with progressive confusion, asterixis, and lethargy over 24 hours. He has been taking furosemide 40 mg daily for ascites management. Vital signs are stable (BP 122/78, HR 88, RR 16, Temp 37.1°C). Laboratory studies show: serum ammonia 156 μmol/L (normal <30), creatinine 0.9 mg/dL, serum potassium 3.1 mEq/L, chloride 92 mEq/L, and bicarbonate 38 mEq/L. Arterial blood gas shows pH 7.48, PaCO2 48 mmHg, HCO3- 38 mEq/L, and PaO2 92 mmHg on room air. Which of the following best explains the worsening of hepatic encephalopathy in this patient?

1. A)Respiratory acidosis increases the pKa of ammonia, promoting conversion to the non-ionized form that crosses the blood-brain barrier
2. B)Metabolic alkalosis promotes renal ammonia excretion, paradoxically increasing systemic ammonia levels
3. C)Metabolic alkalosis shifts ammonia equilibrium toward the non-ionized form, increasing brain penetration and neurotoxicityGABARITO
4. D)Hypokalemia from diuretic use reduces ammonia synthesis in the liver, causing compensatory CNS ammonia accumulation
5. E)The elevated bicarbonate competitively inhibits renal ammonium excretion, reducing ammonia clearance