A 64-year-old man comes to the emergency department with worsening shortness of breath. For the past 3 days, the patient has developed rhinorrhea and cough and thinks he might have contracted something from his grandchildren. He has a 40-pack-year history of smoking with baseline shortness of breath with exertion. The patient also reports bilateral ankle swelling. Physical examination shows a mildly overweight man in mild respiratory distress. Lung auscultation indicates bilateral wheezes and a prolonged expiratory phase. White blood cell count is 14,500/mm3, and hemoglobin level is 16 g/dL. Arterial blood gas analysis shows the following:
| pH | 7.34 |
| PaO2 | 68 mm Hg |
| PaCO2 | 65 mm Hg |
The absence of marked acidosis in this patient is best explained by which of the following?
This patient with probable chronic obstructive pulmonary disease (COPD) (extensive smoking history, progressive respiratory symptoms with wheezing and a prolonged expiratory phase, edema suggestive of possible cor pulmonale) presents with worsening dyspnea and significant hypercapnia (PaCO2 65 mm Hg). Patients with chronic hypoventilation due to COPD, obesity hypoventilation syndrome, or neuromuscular causes have gradual increases in PaCO2 that result in chronic respiratory acidosis; to compensate, the kidneys increase HCO3- retention, creating a chronic secondary metabolic alkalosis. With an acute exacerbation of COPD, the PaCO2 can increase further, as seen in this patient.
Normally, the expected pH resulting from a purely acute increase in PaCO2 from 40 mm Hg (normal) to 65 mm Hg is ~7.20 as pH decreases ~0.08 for every 10 mm Hg of acute increase in PaCO2. This patient's near-normal pH of 7.34 suggests a large component of chronic hypercapnia for which the kidneys have had time to compensate. In contrast to respiratory compensation (occurring within minutes), metabolic compensation by the kidneys requires roughly 72 hours and is evident only in the chronic setting.
In other words, this patient's chronic hypercapnia has shifted his baseline PaCO2 from 40 mm Hg to approximately 60 mm Hg, and baseline serum HCO3- from 24 mEq/L to approximately 32 mEq/L.
(Choice A) The shift of bicarbonate out of and chloride into erythrocytes is integral to carbon dioxide transport throughout the body. This is the initial response to a respiratory acidosis but has a minimal effect on pH compared to renal tubular compensation.
(Choice B) Increased dead space ventilation is the main cause of hypercapnia in COPD and acts to worsen the respiratory acidosis.
(Choice C) Minute ventilation is the product of tidal volume and respiratory rate. The body increases minute ventilation to decrease PaCO2 and compensate for metabolic acidosis. Due to underlying COPD, this patient is unable to significantly increase minute ventilation.
(Choice D) Pulmonary vasoconstriction results from alveolar hypoxia. It can help reduce ventilation-perfusion mismatching within the lung but does not compensate for respiratory acidosis.
Educational objective:
The body compensates for chronic hypercapnia (respiratory acidosis) by increasing renal bicarbonate retention and creating a compensatory chronic metabolic alkalosis. The baseline PaCO2 and serum HCO3- are shifted accordingly.