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Zorluk: OrtaNephrology

A 19-year-old female presents to the university clinic reporting two days of persistent nausea, subjective dizziness, and a continuous buzzing sensation in both ears. She also mentions breathing faster than normal over the last few hours. She recently had a severe viral upper respiratory infection and has been taking an over-the-counter medication for muscle aches and fever.

Vital signs are as follows:
Temperature: 37.2∘C(99.0∘F)37.2^\circ\text{C} (99.0^\circ\text{F})
Blood pressure: 118/76 mmHg118/76 \text{ mmHg}
Heart rate: 112/min112/\text{min}
Respiratory rate: 26/min26/\text{min}
Oxygen saturation: 99%99\% on room air

Laboratory studies are obtained:
TestResult
Sodium141 mEq/L141 \text{ mEq/L}
Potassium3.9 mEq/L3.9 \text{ mEq/L}
Chloride104 mEq/L104 \text{ mEq/L}
Bicarbonate14 mEq/L14 \text{ mEq/L}
Blood urea nitrogen16 mg/dL16 \text{ mg/dL}
Serum creatinine0.8 mg/dL0.8 \text{ mg/dL}
Arterial blood gas analysis on room air reveals:
TestResult
pH7.487.48
pCO2p\text{CO}_219 mmHg19 \text{ mmHg}
pO2p\text{O}_2102 mmHg102 \text{ mmHg}

Which of the following best characterizes this patient's acid-base status?

  1. Mixed primary high anion gap metabolic acidosis and primary respiratory alkalosisCevap
  2. B
    Primary high anion gap metabolic acidosis with appropriate respiratory compensation
  3. C
    Primary respiratory alkalosis with appropriate metabolic compensation
  4. D
    Mixed primary non-anion gap metabolic acidosis and primary respiratory alkalosis
  5. E
    Primary high anion gap metabolic acidosis and primary respiratory acidosis

Cevap

The correct characterization is a mixed primary high anion gap metabolic acidosis and primary respiratory alkalosis.
The correct characterization is a mixed primary high anion gap metabolic acidosis and primary respiratory alkalosis. This patient has a classic presentation of salicylate (aspirin) toxicity, characterized by tinnitus, nausea, and hyperventilation. The acid-base analysis requires three steps: 1) The pH is 7.487.48, indicating alkalemia. 2) The anion gap is 141−(104+14)=23141 - (104 + 14) = 23. Since this is >12>12, a primary high anion gap metabolic acidosis is definitively present. 3) To evaluate for a mixed disorder, Winter's formula must be applied: Expected pCO2=1.5(14)+8=29±2 mmHg\text{Expected } p\text{CO}_2 = 1.5(14) + 8 = 29 \pm 2 \text{ mmHg}. The patient's actual pCO2p\text{CO}_2 is 19 mmHg19 \text{ mmHg}. Because the actual pCO2p\text{CO}_2 is significantly lower than the expected compensatory range, an independent primary respiratory alkalosis is also present.

Adım Adım Çözüm

1
Analyze the pH to determine the most prominent disorder.
The pH is 7.487.48 (>7.40> 7.40), indicating net alkalemia.
Establishing the net pH direction helps frame the primary physiological derangement.
2
Calculate the serum anion gap (AG).
AG=Na+−(Cl−+HCO3−)=141−(104+14)=23\text{AG} = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 141 - (104 + 14) = 23.
An elevated AG (normal 8−12 mEq/L8-12 \text{ mEq/L}) firmly establishes the presence of a primary high anion gap metabolic acidosis, regardless of the overall pH.
3
Calculate the expected respiratory compensation using Winter's formula.
Expected pCO2=1.5×(HCO3−)+8±2=1.5(14)+8±2=29±2 mmHg\text{Expected } p\text{CO}_2 = 1.5 \times (\text{HCO}_3^-) + 8 \pm 2 = 1.5(14) + 8 \pm 2 = 29 \pm 2 \text{ mmHg} (Range: 27−31 mmHg27-31 \text{ mmHg}).
Whenever a metabolic acidosis is identified, you must calculate expected respiratory compensation to rule out hidden mixed disorders.
4
Compare the actual pCO2p\text{CO}_2 to the expected pCO2p\text{CO}_2.
The actual pCO2p\text{CO}_2 is 19 mmHg19 \text{ mmHg}, which is significantly lower than the expected 27−31 mmHg27-31 \text{ mmHg}.
Because the actual pCO2p\text{CO}_2 is driven lower than compensatory levels, the patient has an independent, concurrent primary respiratory alkalosis.

Anahtar Kavram

Patients with salicylate toxicity typically present with a mixed primary respiratory alkalosis (due to direct medullary respiratory center stimulation) and primary high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation).
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