A 4-week-old, full-term boy is brought to the emergency department due to vomiting. His parents describe the emesis as undigested formula without blood or bile. The vomiting occurs after feeds and has increased in frequency and force over the past 3 days. He is afebrile. Blood pressure is normal, pulse is 182/min, and oxygen saturation of 98% on room air. Examination shows a sunken anterior fontanelle and dry mucous membranes. Cardiac examination reveals tachycardia but no murmurs or gallops. The abdomen is soft, nontender, and nondistended. Arterial blood gas analysis is most likely to reveal which of the following sets of values?

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11ec160b_3b58_32fe_9249_8d232ca1637f_MD0001_00 This 4-week-old infant has had severe, nonbilious vomiting (suggesting pyloric stenosis) and now has multiple signs of volume depletion (eg, dry mucous membranes, sunken anterior fontanelle, tachycardia). Primary metabolic alkalosis (elevated pH >7.45, elevated HCO₃⁻ >24 mEq/L) with respiratory compensation (PaCO₂ >40 mm Hg) is the expected acid-base disturbance in such a setting. With vomiting, there is loss of hydrochloric acid (H⁺ and Cl⁻) and fluid volume from the stomach. This causes metabolic alkalosis through multiple mechanisms: The loss of H⁺ ions reduces the amount of carbonic acid (H₂CO₃) buffer in the body and increases the relative quantity of HCO₃⁻. Volume loss and reduced oral intake lead to intravascular volume depletion and decreased renal perfusion, triggering activation of the renin-angiotensin-aldosterone system. Aldosterone stimulates Na⁺ reabsorption in the distal tubules at the expense of increased renal H⁺ and K⁺ excretion. Hypovolemia, hypokalemia, and hypochloremia (from loss of hydrochloric acid) all contribute to impaired renal HCO₃⁻ excretion, leading to increased renal HCO₃⁻ reabsorption. Hypokalemia also causes cells to exchange intracellular K⁺ for extracellular H⁺, which increases serum potassium at the expense of decreased H⁺ concentration (increased blood alkalinity). Treatment of the underlying cause of vomiting and restoration of fluid volume with normal saline (typically with potassium repletion) is needed to resolve the hypokalemic, hypochloremic metabolic alkalosis. (Choice A) Low pH and low HCO₃⁻ indicate metabolic acidosis, which can have a normal (eg, due to diarrhea or renal tubular acidosis) or elevated anion gap. PaCO₂ is low due to respiratory compensation. (Choice B) Low pH and elevated PaCO₂indicate respiratory acidosis. The near-normal HCO₃⁻ is consistent with minimal metabolic compensation, suggesting the respiratory acidosis is acute (eg, due to hypoventilation from opioid overdose). (Choice C) These acid-base values are considered normal, indicating an absence of acid-base disturbance. (Choice E) High pH and elevated HCO₃⁻ indicate metabolic alkalosis, with elevated PaCO₂ indicating respiratory compensation (as expected in this patient). Metabolic alkalosis can also be associated with small increases in the serum anion gap due to release of H⁺ from albumin (buffering effect that increases albumin's anionic charge). Educational objective: Severe vomiting leads to metabolic alkalosis through multiple mechanisms, including loss of H⁺ from the gastrointestinal tract, volume and Cl⁻ depletion that induces renal retention of HCO₃⁻, and hypokalemia-induced intracellular shifting of H⁺. __________ References: Physiology, metabolic alkalosis. (http://www.ncbi.nlm.nih.gov/pubmed/29493916)

A 4-Week-Old, Full-Term Boy Is Brought to the Emergency Department