Situation: A 34-year-old man who works outdoors comes to the emergency room with sudden, severe right flank pain spreading to the groin that began 2 hours ago. He is pacing, breathing rapidly at 32/min, and reports tingling of his fingers and around his lips. Temperature is 37.0 °C, blood pressure 138/86 mmHg, and pulse 104/min. His urinalysis shows red blood cells with negative nitrite and leukocyte esterase, and his creatinine is 0.9 mg/dL (80 µmol/L). A computed tomography (CT) scan shows a 4-mm stone in the lower ureter. His arterial blood gas (ABG) results on room air are (PaCO2 = partial pressure of carbon dioxide in arterial blood; HCO3− = bicarbonate): pH 7.52 PaCO2 29 mmHg HCO3− 23 mEq/L (Reference ranges: pH 7.35–7.45; PaCO2 35–45 mmHg; HCO3− 22–26 mEq/L) How should the nurse interpret these results?

The pH of 7.52 shows alkalosis. The PaCO2 of 29 mmHg is low and explains the alkaline pH, so the primary problem is respiratory alkalosis from pain-driven hyperventilation. The HCO3− of 23 mEq/L is within the 22–26 mEq/L range, so the kidneys have not yet compensated, which is expected because renal compensation takes hours to days.

Step 1 — Identify the primary acid–base disorder

The arterial blood gas shows a pH of 7.52, which is above the reference range of 7.35–7.45, indicating alkalosis. The PaCO₂ is 29 mmHg, which is below the normal range of 35–45 mmHg. A low PaCO₂ means the patient is blowing off carbon dioxide, and this respiratory change directly raises the pH. Therefore, the primary problem is respiratory alkalosis.

The pH and PaCO₂ move in opposite directions in respiratory alkalosis: pH is high while PaCO₂ is low. This is the hallmark of a primary respiratory disorder, not a metabolic one.

Step 2 — Determine whether compensation has begun

The HCO₃⁻ is 23 mEq/L, which falls within the normal range of 22–26 mEq/L. In respiratory alkalosis, the kidneys would normally compensate by excreting bicarbonate to lower the pH back toward normal. Because the bicarbonate is still normal, no renal compensation has occurred yet.

Renal compensation for respiratory alkalosis takes hours to days to develop, so a normal HCO₃⁻ in the acute setting indicates an uncompensated state. The patient’s symptoms began only 2 hours ago, which is far too early for meaningful renal compensation.

Step 3 — Connect the ABG to the clinical picture

This patient has a 4-mm stone in the lower ureter causing severe flank pain radiating to the groin. Acute pain is a powerful driver of hyperventilation. His respiratory rate is 32/min, and he reports perioral and digital tingling. These symptoms are classic manifestations of acute respiratory alkalosis: rapid breathing lowers PaCO₂, which reduces ionized calcium levels and produces paresthesias.

Key point! Tingling around the lips and fingers in a hyperventilating patient points to respiratory alkalosis, not a primary calcium disorder. The ABG confirms the mechanism.

Step 4 — Compare with the other options

Option	Why it is incorrect
1. Metabolic alkalosis, uncompensated	Metabolic alkalosis would show a high HCO₃⁻ as the primary change. Here HCO₃⁻ is normal, and the low PaCO₂ is the primary abnormality.
3. Metabolic alkalosis, partially compensated	Same problem: HCO₃⁻ is not elevated, so metabolic alkalosis is not present. Also, compensation would require an abnormal HCO₃⁻ moving in the opposite direction.
4. Respiratory alkalosis, partially compensated	Partially compensated respiratory alkalosis would show a decreased HCO₃⁻ as the kidneys begin to excrete bicarbonate. Here HCO₃⁻ remains within normal limits.

Step 5 — Why acute pain causes this specific ABG pattern

The ureteral stone triggers intense visceral pain transmitted through sympathetic and parasympathetic pathways. Pain activates the respiratory centers in the brainstem, increasing both respiratory rate and depth. This blows off CO₂ faster than the body produces it, lowering PaCO₂ and raising pH. The kidneys cannot respond quickly because renal compensation requires changes in bicarbonate reabsorption and excretion that develop over 6–24 hours or longer.

Watch out! Do not confuse the normal HCO₃⁻ with “no acid–base problem.” The normal bicarbonate is exactly what defines this as uncompensated respiratory alkalosis.

Step 6 — Clinical relevance for nursing care

The nurse should recognize that the ABG abnormality is a consequence of pain and hyperventilation, not a primary pulmonary or metabolic disease. The priority is to treat the underlying pain from the ureteral stone. As pain is controlled, the respiratory rate will slow, PaCO₂ will rise, and the pH will normalize. The normal creatinine of 0.9 mg/dL and negative nitrite/leukocyte esterase suggest that renal function is intact and there is no urinary tract infection, which supports a straightforward pain-driven respiratory alkalosis.

The presence of red blood cells in the urine with a normal creatinine and no signs of infection is consistent with an uncomplicated ureteral stone, and the ABG disturbance is secondary to the pain response.