A 67-year-old man comes to the emergency department due to cough with greenish sputum production and increased shortness of breath over the last 4 days. His medical history includes chronic obstructive pulmonary disease treated with tiotropium and budesonide/formoterol. The patient reports increased use of albuterol to 4 times a day. Two months ago, his FEV1 to FVC ratio was 55% of predicted and diffusing capacity of the lungs for carbon monoxide was within normal limits. Today, the patient's blood pressure is 152/90 mm Hg, pulse is 108/min, respirations are 22/min, and pulse oximetry shows 88% on room air. He is in mild respiratory distress with some accessory muscle usage and can speak in short sentences. Chest auscultation reveals prolonged expiration with bilateral wheezes. Arterial blood gas on room air shows pH 7.35, PaCO₂ 44 mm Hg, and PaO₂ 55 mm Hg. Pulse oximetry improves to 95% after he is placed on supplemental oxygen at 5 L/min. Which of the following mechanisms best explains this patient's improvement in oxygen saturation following oxygen supplementation?

Question

Quizplus · Accepted Answer

Explanation: Hypoxemia in chronic obstructive pulmonary disease (COPD) is primarily caused by ventilation/perfusion (V/Q) mismatch. The emphysematous component of COPD causes airflow limitation due to loss of elastic tissue and small bronchiolar collapse, and chronic bronchitis contributes to airflow limitation as well. COPD exacerbation causes further airflow limitation due to mucus plugging and bronchospasm. The result is numerous localized areas of lung that have a low V/Q ratio, which is the major cause of hypoxemia in patients with COPD. These poorly ventilated lung regions (low V/Q regions) undergo hypoxic vasoconstriction to improve overall gas exchange efficiency, but nonetheless still have a low V/Q ratio. Despite restricted airflow, supplemental oxygen (O₂) is able to successfully reach the alveoli in these regions, resulting in an increase in Q (due to alleviation of hypoxic vasoconstriction) and improved gas exchange to the blood (improved hypoxemia). Emphysema also leads to areas of lung that have a high V/Q ratio (dead space ventilation) due to destruction of the alveolar-capillary interface, but these regions play a relatively minor role in hypoxemia and are more important in the development of hypercapnia. Supplemental O₂ also increases V in high V/Q lung regions; however, as Q does not increase significantly (and the O₂-carrying capacity of existing Q is essentially maxed out), the ability to improve hypoxemia from these regions is minimal (Choice C). (Choice A) Right-to-left anatomic shunts (eg, cyanotic congenital heart disease) bypass normal pulmonary capillary beds. Because blood is never delivered to the alveoli, increasing alveolar O₂ content will not alter systemic oxygenation. (Choice B) Increased fraction of inspired O₂ increases the O₂ partial pressure gradient across the alveolar-pulmonary capillary membrane, resulting in increased diffusing capacity of the lung for O₂. However, the effects on hypoxemia are minimal compared to those of improved V/Q mismatch. (Choice E) When O₂ binds to hemoglobin, it promotes the release of carbon dioxide from hemoglobin (Haldane effect); however, the effect on hypoxemia of increased off-loading of carbon dioxide is not significant. Haldane effect Educational objective: Ventilation/perfusion (V/Q) mismatch in low V/Q lung regions is the major cause of hypoxemia in patients with chronic obstructive pulmonary disease, and the mismatch is worsened during exacerbation. Supplemental oxygen improves hypoxemia in these patients primarily by increasing oxygen exchange in lung regions that have a low V/Q ratio. References: Gas exchange and ventilation-perfusion relationships in the lung. (http://www.ncbi.nlm.nih.gov/pubmed/25063240) Hypoxemia in patients with COPD: cause, effects, and disease progression. (http://www.ncbi.nlm.nih.gov/pubmed/21660297)

A 67-Year-Old Man Comes to the Emergency Department Due to Cough