A 37-year-old man comes to the emergency department due to progressive weakness. He has been vomiting everything he eats for the past 4 days. The patient's medical history is significant for Helicobacter pylori infection, but he never completed pharmacotherapy. He smokes 1 pack of cigarettes daily and drinks 3-4 beers every day. Blood pressure is 100/70 mm Hg, pulse is 104/min, and respirations are 12/min. Oxygen saturation is 95% on room air. Mucous membranes are dry, and the physical examination is otherwise unremarkable. Which of the following changes are most likely in this patient?

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Explanation: 11ec25c8_d959_a3a2_bc81_fd31cafbc608_MD0003_00 This patient has had severe vomiting (possibly due to an untreated peptic ulcer) and now has evidence of volume depletion (eg, dry mucous membranes, tachycardia). Vomiting causes a significant loss of gastric H⁺ from the body. It also causes loss of water and salt (NaCl), with relatively more loss of Cl^- than Na⁺ due to the high gastric quantity of hydrochloric acid (HCl). These losses trigger characteristic electrolyte abnormalities resulting in hypokalemic, hypochloremic metabolic alkalosis. ⁺ ^- ⁺ HCl The loss of H⁺ reduces the amount of carbonic acid (H₂CO₃) buffer in the body, resulting in an increase in the relative quantity of bicarbonate (HCO₃^-). Metabolic alkalosis is initiated with increased serum HCO₃^-. Volume loss decreases renal perfusion and activates the renin-angiotensin-aldosterone system. The secondary hyperaldosteronism stimulates Na⁺ reabsorption in the distal tubules at the expense of increased K⁺ and H⁺ excretion. This leads to hypokalemia and worsens the metabolic alkalosis. The loss of Cl^- from the stomach and kidneys (which is relatively greater than the passive Cl^- reabsorption that aldosterone stimulates along with Na⁺ reabsorption) leads to profound total body Cl^- depletion and hypochloremia. Because adequate Cl^- delivery to the distal renal tubules is required for appropriate excretion of HCO₃^- (via the pendrin exchanger), the Cl^- depletion causes impaired HCO₃^- excretion and perpetuates the metabolic alkalosis. Urine sodium and urine chloride are low due to total body depletion and aldosterone-mediated renal tubular reabsorption. Clinically, low urine chloride is an important indicator of the etiology and appropriate treatment of metabolic alkalosis. It is the expected finding in etiologies of metabolic alkalosis that are primarily driven by Cl^- depletion (eg, severe vomiting, diuretic overuse), and indicates that repletion of volume and Cl^- with normal saline will shut off the mechanisms perpetuating the alkalosis and allow serum electrolytes to normalize (saline responsive). ^- ^- Educational objective: Severe vomiting characteristically causes hypokalemic, hypochloremic metabolic alkalosis. The metabolic alkalosis is initiated by loss of gastric H⁺, worsened by hypovolemia-induced activation of the renin-angiotensin-aldosterone system, and perpetuated by profound total body Cl^- depletion leading to hypochloremia and impaired renal bicarbonate excretion. Urine Na⁺ and Cl^- are low due to total body depletion and aldosterone-mediated renal tubular reabsorption. Repletion of volume and Cl^- with normal saline corrects the metabolic alkalosis (saline responsive). ⁺ ^- ⁺ ^- ^- References: Approach to metabolic alkalosis. (http://www.ncbi.nlm.nih.gov/pubmed/24766943)

A 37-Year-Old Man Comes to the Emergency Department Due to Progressive