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Zorluk: OrtaNephrology

A 21-year-old woman is brought to the emergency department by her college roommate due to confusion, nausea, and ringing in her ears for the past 6 hours. The roommate reports that the patient was distraught over a recent breakup and may have ingested "a bottle of pills." On physical examination, her temperature is 38.0°C (100.4°F), blood pressure is 115/75 mm Hg, pulse is 112/min, and respiratory rate is 28/min. The patient appears flushed and is breathing deeply and rapidly. Lungs are clear to auscultation bilaterally. Laboratory results show:

Serum sodium: 140 mEq/L
Serum potassium: 3.6 mEq/L
Serum chloride: 102 mEq/L
Serum bicarbonate: 16 mEq/L
Blood urea nitrogen: 14 mg/dL
Serum creatinine: 0.8 mg/dL

Arterial blood gas (room air):
pH: 7.48
PaCO2PaCO_2: 22 mm Hg
PaO2PaO_2: 100 mm Hg

Which of the following best describes this patient's current acid-base derangement?

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

Cevap

Mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis
The correct answer accurately synthesizes the laboratory data into a mixed disorder. The patient's alkalemic pH (7.48) and low PaCO2PaCO_2 (22 mm Hg) indicate a primary respiratory alkalosis. However, calculating the anion gap yields a value of 22 mEq/L (140−[102+16]140 - [102 + 16]), which confirms the presence of a concurrent primary high anion gap metabolic acidosis. This mixed acid-base derangement is the classic hallmark of salicylate (aspirin) toxicity, consistent with her tinnitus, tachypnea, fever, and history of pill ingestion.

Adım Adım Çözüm

1
Analyze the pH to determine the predominant acid-base status.
The pH is 7.48, indicating alkalemia.
Establishing alkalemia (pH > 7.45) directs us to look for a primary alkalosis.
2
Identify the primary process driving the alkalemia by looking at the PaCO2PaCO_2 and HCO3−HCO_3^-.
The PaCO2PaCO_2 is low at 22 mm Hg. A low PaCO2PaCO_2 causes alkalemia, so the primary disorder is a respiratory alkalosis.
Since the HCO3−HCO_3^- is low (16 mEq/L), it cannot be the cause of the alkalemia; rather, it suggests either compensation or a concurrent metabolic acidosis.
3
Calculate the expected metabolic compensation for the acute respiratory alkalosis.
In acute respiratory alkalosis, HCO3−HCO_3^- drops by 2 mEq/L for every 10 mm Hg drop in PaCO2PaCO_2. The PaCO2PaCO_2 dropped by 18 (from 40 to 22). Expected HCO3−HCO_3^- drop = 18×(2/10)=3.618 \times (2/10) = 3.6. Expected HCO3−≈24−3.6=20.4HCO_3^- \approx 24 - 3.6 = 20.4 mEq/L.
Because the actual HCO3−HCO_3^- (16 mEq/L) is significantly lower than the expected compensated value (20.4 mEq/L), there must be an additional primary metabolic acidosis.
4
Calculate the serum anion gap to classify the metabolic acidosis.
AnionGap=Na+−(Cl−+HCO3−)=140−(102+16)=140−118=22Anion Gap = Na^+ - (Cl^- + HCO_3^-) = 140 - (102 + 16) = 140 - 118 = 22 mEq/L.
An anion gap > 12 mEq/L confirms the presence of a high anion gap metabolic acidosis (HAGMA).
5
Alternatively, check Winter's formula starting from the metabolic acidosis.
Expected PaCO2=1.5×[HCO3−]+8±2=1.5×16+8=32±2PaCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2 = 1.5 \times 16 + 8 = 32 \pm 2 mm Hg. The actual PaCO2PaCO_2 (22 mm Hg) is much lower than the 30-34 mm Hg range.
This alternate calculation confirms that the respiratory alkalosis is a primary disorder, not just compensation for the HAGMA.

Anahtar Kavram

Salicylate toxicity classically presents 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 and accumulation of organic acids).
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