A 45-year-old man comes to the emergency department due to severe dyspnea and chest discomfort that began earlier in the day. The dyspnea has been worsening throughout the day and has been present at rest. He reports no inciting trauma. The patient has no other medical conditions and takes no medications. He has a 20-pack-year smoking history and does not use alcohol or illicit drugs. Temperature is 36.7 C (98 F), blood pressure is 110/60 mm Hg, and pulse is 96/min. Arterial blood gas drawn on room air shows an arterial partial pressure of oxygen (PaO₂) of 54 mm Hg and an arterial partial pressure of carbon dioxide (PaCO₂) of 26 mm Hg. Which of the following processes is most likely occurring in this patient?

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11ec160b_3b4c_7319_9249_d1a078344337_MD0001_00 This patient with acute-onset dyspnea and chest discomfort likely has an acute pulmonary embolism (PE). PE leads to increased dead-space ventilation with a consequent ventilation/perfusion (V/Q) mismatch that causes hypoxemia. The acute hypoxemia along with pulmonary parenchymal inflammation triggers an increase in respiratory drive and hyperventilation. Because the rate of CO₂removal is closely tied to ventilation rate, alveolar hyperventilation leads to increased expiration of CO₂ with resulting hypocapnia (low arterial partial pressure of carbon dioxide [PaCO₂]) and respiratory alkalosis. In contrast, the rate of O₂ absorption becomes capped once hemoglobin is saturated, which occurs at relatively low arterial partial pressure of oxygen (PaO₂) levels (eg, hemoglobin is 85% saturated at PaO₂ 50 mm Hg). Therefore, the blood in highly ventilated lung regions cannot absorb extra O₂ to compensate for poorly ventilated regions, and hyperventilation does not significantly increase PaO₂. It follows that patients with an acute V/Q mismatch (eg, due to PE or pneumonia) typically have hypocapnia with respiratory alkalosis and persistent hypoxemia. Without treatment, prolonged hyperventilation can lead to respiratory muscle fatigue (Choice E) with consequent respiratory failure; these patients will have hypoventilation with hypercapnia and respiratory acidosis. (Choices B and D) Both decreased chest wall compliance, as occurs in obesity hypoventilation syndrome, and poor respiratory drive, as occurs in opioid overdose and some types of stroke, lead to hypoventilation with hypoxemia and increased PaCO₂ levels. (Choice C) Expiratory air trapping occurs in chronic obstructive lung disease. These patients often have chronic respiratory acidosis (high PaCO₂) that may worsen (acute on chronic respiratory acidosis) during exacerbation. Educational objective: An acute ventilation/perfusion mismatch (eg, due to pulmonary embolism or pneumonia) causes hypoxemia and triggers hyperventilation. Because the removal of CO₂ is directly dependent on ventilation but the absorption of O₂ is capped by the high baseline saturation of hemoglobin, the hyperventilation response typically leads to respiratory alkalosis (low arterial partial pressure of carbon dioxide) with persistent hypoxemia. __________ References: Mechanisms of hypoxemia and hypocapnia in pulmonary embolism. (http://www.ncbi.nlm.nih.gov/pubmed/7599843)

A 45-Year-Old Man Comes to the Emergency Department Due to Severe