Metabolic Alkalosis with Respiratory Compensation
This patient has metabolic alkalosis with respiratory compensation (Answer D). The clinical picture and laboratory values definitively demonstrate a primary metabolic alkalosis with appropriate respiratory compensation through hypoventilation.
Systematic Analysis of Acid-Base Status
Primary Disorder Identification
The elevated pH (7.56) confirms alkalemia, which narrows the diagnosis to either metabolic alkalosis or respiratory alkalosis as the primary process 1.
The markedly elevated bicarbonate (42 mEq/L, normal 22-26) indicates metabolic alkalosis as the primary disorder, as bicarbonate is the metabolic component of acid-base balance 1.
The elevated PCO2 (50 mm Hg, normal 35-45) represents respiratory compensation, not a primary respiratory disorder, as the body attempts to normalize pH by retaining CO2 through hypoventilation 2, 3.
Distinguishing Compensation from Mixed Disorder
In a simple metabolic alkalosis, the expected compensatory increase in PCO2 is approximately 0.7 mm Hg for every 1 mEq/L increase in bicarbonate 3, 4. With bicarbonate elevated by 18 mEq/L (42-24), the expected PCO2 would be approximately 40 + (0.7 × 18) = 52.6 mm Hg, which closely matches the observed PCO2 of 50 mm Hg.
This appropriate degree of respiratory compensation confirms a simple metabolic alkalosis with compensation, not a combined or mixed disorder 3, 5.
Clinical Context Supporting the Diagnosis
Mechanism of Metabolic Alkalosis
Prolonged nasogastric suction causes loss of gastric hydrochloric acid (HCl), directly generating metabolic alkalosis by removing hydrogen ions and chloride from the body 4.
The extremely low urine chloride (6 mEq/L) confirms chloride-responsive (contraction) alkalosis, indicating volume depletion and appropriate renal bicarbonate retention 1.
Volume depletion from inadequate fluid replacement activates the renin-angiotensin-aldosterone system, promoting renal sodium and bicarbonate reabsorption while excreting potassium and hydrogen ions, perpetuating the alkalosis 1.
Supporting Laboratory and Clinical Findings
Hypokalemia (3.1 mEq/L) is characteristic of metabolic alkalosis, as alkalemia shifts potassium intracellularly and aldosterone activation increases urinary potassium losses 6, 4.
Hypochloremia (80 mEq/L) results from gastric losses and renal chloride conservation in response to volume depletion 4.
The low urine sodium (2 mEq/L) reflects avid renal sodium retention in response to volume depletion, a hallmark of contraction alkalosis 1.
Physical examination findings of diminished skin turgor, dry mucous membranes, and orthostatic hypotension confirm significant volume depletion 7.
Why Other Options Are Incorrect
Option A (Uncompensated metabolic alkalosis) is incorrect because the elevated PCO2 demonstrates clear respiratory compensation; uncompensated alkalosis would show normal PCO2 3.
Option B (Respiratory acidosis with metabolic compensation) is incorrect because the pH is alkalemic (7.56), not acidemic, ruling out any primary acidosis 2, 4.
Option C (Combined metabolic and respiratory alkalosis) is incorrect because the elevated PCO2 represents acidosis (compensation), not alkalosis; combined alkalosis would show low PCO2 and high bicarbonate driving pH even higher 3, 5.
Option E (Mixed respiratory acidosis and respiratory alkalosis) is physiologically impossible, as one cannot simultaneously hypoventilate and hyperventilate 3.
Critical Clinical Pitfalls
Do not confuse appropriate respiratory compensation with a primary respiratory disorder—the key is that compensation never fully normalizes pH, and the PCO2 change is proportionate to the bicarbonate change 3, 4.
Do not overlook the clinical context: prolonged NG suction with volume depletion is a classic setup for contraction alkalosis, and the urine electrolytes (very low chloride and sodium) confirm the diagnosis 1, 4.
Recognize that the slightly low sodium (132 mEq/L) represents dilutional hyponatremia from volume depletion, not true sodium deficit, as evidenced by the avid renal sodium retention 1.