A diabetic woman is admitted due to persistent vomiting. She gives a history of consuming food from outside. On evaluation, her blood pressure is 90/60 mmHg. Her arterial blood gas (ABG) report shows the following findings. What is the cause of her ABG findings? pH-7.52 HCO3 – 30 meq/L PaCO2 - 20 mmHg Na – 123 mEq/L K – 3.2 mEq/L CI – 67 mEq/L

Correct Answer: C. Persistent vomiting

The ABG pattern shows metabolic alkalosis with respiratory compensation (pH 7.52, HCO3 30, PaCO2 20). The clinical context—persistent vomiting, hypotension (90/60), hyponatremia (Na 123), hypokalemia (K 3.2), and hypochloremia (Cl 67)—is pathognomonic for loss of gastric acid and electrolytes through vomiting. Gastric juice contains HCl, K+, and Cl−; loss of this acidic fluid causes metabolic alkalosis. The low PaCO2 represents respiratory compensation (hyperventilation) to lower pH. Hyponatremia and hypokalemia occur due to volume depletion and renal losses triggered by alkalosis (increased aldosterone activity). The hypotension reflects hypovolemia from fluid loss. In a diabetic patient with food from outside, one might initially suspect DKA, but DKA produces metabolic acidosis (low pH, low HCO3), not alkalosis. The electrolyte pattern—specifically the triad of hypokalemia, hypochloremia, and hyponatremia with alkalosis—is the hallmark of contraction alkalosis from vomiting. This is a classic presentation in Indian clinical practice, particularly in patients with gastroenteritis or persistent vomiting.

Why the other options are wrong

A. Septic shock — Septic shock typically causes metabolic acidosis (low pH, low HCO3) due to tissue hypoperfusion and lactate accumulation, not alkalosis. While hypotension is present, the ABG shows alkalosis with elevated HCO3—opposite of sepsis. Sepsis would also show elevated lactate and different electrolyte derangements. The clinical context of vomiting, not infection, is the key discriminator. B. Renal tubular acidosis — RTA causes metabolic acidosis (low pH, low HCO3) due to impaired renal acid excretion or bicarbonate reabsorption, not alkalosis. The patient's pH is elevated (7.52) and HCO3 is high (30), which is the opposite of RTA. RTA does not explain the acute presentation with vomiting or the severe electrolyte losses (Na, K, Cl) seen here. D. Diabetic ketoacidosis — DKA produces metabolic acidosis (low pH, low HCO3, elevated anion gap) due to ketone accumulation, not alkalosis. This patient's pH is 7.52 (alkalemic) and HCO3 is 30 (elevated)—the opposite of DKA. While the patient is diabetic and has vomiting, the ABG pattern rules out DKA. DKA would show low pH and low HCO3, not the pattern seen here.

High-Yield Facts

Mnemonics

VOMIT = Vomiting-induced alkalOsis Memory Vomiting → Outflow of HCl → Metabolic alkalosis → Ion loss (K, Na, Cl) → Therapy (IV fluids + K+ replacement). Use when you see alkalosis + vomiting history. ABG in Vomiting: HIGH-LOW-LOW HIGH pH (alkalemia), LOW PaCO2 (respiratory compensation), LOW K/Cl/Na (electrolyte losses). Differentiates from DKA (low pH) and RTA (acidosis).

NBE Trap

NBE pairs a diabetic patient with vomiting and hypotension to lure students toward DKA; however, the alkalotic ABG (pH 7.52, HCO3 30) rules out DKA, which always presents with acidosis. The trap is recognizing that vomiting, not diabetes, is the primary driver of the ABG abnormality here.

Clinical Pearl

In Indian emergency departments, persistent vomiting from gastroenteritis (common in monsoon season) is a leading cause of metabolic alkalosis and hypokalemia-induced arrhythmias. Always check serum K+ and Cl− in vomiting patients; IV normal saline + KCl replacement is the standard DOC, not bicarbonate therapy.

_Reference: Harrison Ch. 48 (Acid-Base Disorders); Robbins Ch. 3 (Fluid, Electrolyte, and Acid-Base Disorders); KD Tripathi Ch. 8 (Electrolyte and Acid-Base Balance)_