A 60-year-old woman comes to the emergency department due to shortness of breath and productive cough. The patient has a 30-pack-year smoking history. Oxygen saturation is 88% on room air. On physical examination, she appears uncomfortable and uses her accessory respiratory muscles to breathe. Expiratory wheezes are heard throughout the lungs. The patient is started on high-flow oxygen supplementation. Shortly afterward, she becomes increasingly lethargic and confused. This patient's clinical decline is most likely attributable to an increase in which of the following parameters?

Question

A 60-year-old woman comes to the emergency department due to shortness of breath and productive cough.  The patient has a 30-pack-year smoking history.  Oxygen saturation is 88% on room air.  On physical examination, she appears uncomfortable and uses her accessory respiratory muscles to breathe.  Expiratory wheezes are heard throughout the lungs.  The patient is started on high-flow oxygen supplementation.  Shortly afterward, she becomes increasingly lethargic and confused.  This patient's clinical decline is most likely attributable to an increase in which of the following parameters?

Quizplus · Accepted Answer

11ec160b_3b34_7f17_9249_e709f2b531dc_MD0001_00 This patient's clinical presentation (ie, dyspnea, productive cough, hypoxemia, expiratory wheezing, accessory muscle use, smoking history) is consistent with a chronic obstructive pulmonary disease (COPD) exacerbation. Supplemental oxygen may be warranted in patients with COPD who have significant hypoxemia; however, administration of excessively high oxygen concentrations can lead to increased CO₂ retention (oxygen-induced hypercapnia), resulting in confusion and a depressed level of consciousness (eg, lethargy). Several mechanisms contribute to oxygen-induced hypercapnia, but the major cause is increased ventilation-perfusion mismatch. Hypoxia causes vasoconstriction of the pulmonary arterioles, which acts to shunt blood toward alveoli with the highest ventilation, thereby minimizing physiologic dead space. Providing high-concentration supplemental oxygen allows lung regions with relatively poor ventilation to have higher oxygen levels, reversing pulmonary vasoconstriction. The redistribution of blood flow away from well-ventilated alveoli leads to an increase in physiologic dead space (well-ventilated alveoli are less perfused) with a corresponding reduction in CO₂ excretion. (Choice A) Oxygen administration alleviates hypoxic pulmonary vasoconstriction, causing an overall decrease in pulmonary vascular resistance. (Choice B) Hyperoxia can increase production of reactive oxygen species (eg, superoxide, hydroxyl radical, hydrogen peroxide), leading to injury of the airways and lung parenchyma. Oxygen toxicity typically manifests with substernal heaviness, pleuritic chest pain, and cough/dyspnea within 24 hours after breathing pure oxygen. (Choice C) In patients with hypercapnia and respiratory acidosis, the kidneys compensate by increasing bicarbonate reabsorption and normalizing the serum pH level. This response occurs slowly over several days and would tend to ameliorate the effects of hypercapnia. (Choice D) Peripheral chemoreceptors in the carotid and aortic bodies sense arterial PaO₂ and are normally stimulated by hypoxemia. High-flow oxygen reduces chemoreceptor stimulation, resulting in a decreased (not increased) respiratory rate and minute ventilation. Educational objective: Supplemental oxygen administration in patients with chronic obstructive pulmonary disease can lead to increased CO₂ retention (oxygen-induced hypercapnia), resulting in confusion and depressed consciousness. The major cause is reversal of hypoxic pulmonary vasoconstriction, which increases physiologic dead space as blood is shunted away from well-ventilated alveoli. __________ References: Oxygen-induced hypercapnia in COPD: myths and facts. (http://www.ncbi.nlm.nih.gov/pubmed/23106947)

A 60-Year-Old Woman Comes to the Emergency Department Due to Shortness