A 28-year-old woman, gravida 3 para 2, at 31 weeks gestation comes to the office for a prenatal visit. The patient has had increasing shortness of breath while climbing stairs and during long walks for the past few weeks but has had no cough, sick contacts, hemoptysis, orthopnea, or chest pain. She has had no contractions or vaginal bleeding, and fetal movement is normal. The patient has no chronic medical conditions, and her pregnancy has been uncomplicated. Blood pressure is 110/80 mm Hg, pulse is 70/min, and respirations are 18/min. Fetal heart tones are normal. Cardiac examination reveals no rubs or murmurs. The lungs are clear to auscultation bilaterally. The remainder of the examination is unremarkable. Which of the following laboratory findings will most likely be found in this patient?

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11ec160b_3b23_b614_9249_b71d95839e2d_MD0001_00 The normal physiology of pregnancy involves chronic hyperventilation. Elevated progesterone levels trigger a sensation of shortness of breath and stimulate the hypothalamus to increase respiratory drive. Ventilation is increased primarily via increased tidal volume, which is facilitated by increased diaphragmatic excursion and hormone-induced laxity of the intercostal muscles that allows for enlargement of the thoracic cavity (although the expanding uterus displaces the resting position of the diaphragm upward, diaphragmatic excursion is not impaired). A slight increase in respiratory rate also contributes. The hyperventilation of pregnancy creates an expected respiratory alkalosis (ie, pH >7.45 and partial pressure of carbon dioxide in arterial blood [PaCO₂] <40 mm Hg) with metabolic compensation (increased renal bicarbonate [HCO₃⁻] excretion). Arterial oxygenation is also increased slightly above normal (ie, arterial partial pressure of oxygen [PaO₂] >100 mm Hg). These changes help facilitate the transport of acidic wastes from, and the transport of oxygen to, the developing fetus. (Choice A) Low pH (<7.35) with elevated PaCO₂(>40 mm Hg) indicates respiratory acidosis. Urine HCO₃⁻ is low as the kidneys increase HCO₃⁻ reabsorption for metabolic compensation. (Choice B) Low pH is not explained by low PaCO₂ (<40 mm Hg); therefore, the low PaCO₂ likely represents respiratory compensation for metabolic acidosis. Renal loss of HCO₃⁻ (ie, high urine HCO₃⁻), as occurs with renal tubular acidosis, is a common cause of metabolic acidosis. (Choice D) High pH (>7.45) is not explained by elevated PaCO₂; therefore, the elevated PaCO₂ likely represents respiratory compensation for metabolic alkalosis. Renal retention of HCO₃⁻ (ie, low urine HCO₃⁻), as occurs with severe vomiting and diuretic overuse, commonly contributes to metabolic alkalosis. (Choice E) High pH with low PaCO₂ indicates respiratory alkalosis. Urine HCO₃⁻ may be low in the acute setting but begins to increase after several hours to provide metabolic compensation (full metabolic compensation requires approximately 72 hours). This patient at 31 weeks gestation will have fully compensated respiratory alkalosis with increased urine HCO₃⁻ excretion. Educational objective: The normal physiology of pregnancy involves chronic hyperventilation caused by elevated progesterone levels stimulating an increase in central respiratory drive. This creates an expected respiratory alkalosis with metabolic compensation (increased renal bicarbonate excretion) that helps facilitate the transport of acidic wastes from, and the transport of oxygen to, the developing fetus.

A 28-Year-Old Woman, Gravida 3 Para 2, at 31 Weeks