A 28-year-old previously healthy man comes to the urgent care clinic due to shortness of breath. The patient is on a ski vacation in Breckenridge, Colorado, which is situated at an altitude of 2926 m (9600 ft). On arrival 4 days ago, he experienced mild headache and nausea that resolved spontaneously, but since yesterday, he has had worsening dyspnea and cough. The patient now feels short of breath even with minimal exertion. Temperature is 37.3 C (99.1) F, blood pressure is 134/82 mm Hg, pulse is 98/min, and respirations are 22/min. Oxygen saturation is 86% on ambient air, which rapidly improves to 95% with supplemental oxygen. Physical examination shows pink mucous membranes, flat neck veins, bilateral inspiratory crackles, and no heart murmurs or pedal edema. Chest x-ray reveals patchy alveolar infiltrates. Which of the following is the most likely cause of this patient's current condition?

Question

A 28-year-old previously healthy man comes to the urgent care clinic due to shortness of breath.  The patient is on a ski vacation in Breckenridge, Colorado, which is situated at an altitude of 2926 m (9600 ft).  On arrival 4 days ago, he experienced mild headache and nausea that resolved spontaneously, but since yesterday, he has had worsening dyspnea and cough.  The patient now feels short of breath even with minimal exertion.  Temperature is 37.3 C (99.1) F, blood pressure is 134/82 mm Hg, pulse is 98/min, and respirations are 22/min.  Oxygen saturation is 86% on ambient air, which rapidly improves to 95% with supplemental oxygen.  Physical examination shows pink mucous membranes, flat neck veins, bilateral inspiratory crackles, and no heart murmurs or pedal edema.  Chest x-ray reveals patchy alveolar infiltrates.  Which of the following is the most likely cause of this patient's current condition?

Quizplus · Accepted Answer

11ec160b_3b38_9dd1_9249_f5176936ec14_MD0001_00 This patient with dyspnea, hypoxemia, and patchy alveolar infiltrates shortly after arriving at high altitude likely has high-altitude pulmonary edema (HAPE). HAPE can occur within several days of arrival at an altitude >2,500 m (~8,000 ft), with the risk increasing as altitude increases. The pathophysiology is driven by the reduced partial pressure of oxygen (PiO₂) at high altitude, which leads to hypoxic pulmonary vasoconstriction and consequent increased pulmonary arterial pressure. In some individuals with genetic predisposition, the hypoxic vasoconstriction is unevenly distributed, exposing the capillary beds in relatively less vasoconstricted areas to high perfusion pressure. This causes alveolar-capillary membrane disruption and leads to patchy, bilateral pulmonary edema. HAPE typically presents with dyspnea (progressive over 1-2 days) and cough (sometimes with hemoptysis). Accompanying symptoms of acute mountain sickness (eg, headache, nausea) are often present, and physical examination reveals bilateral lung crackles. The hypoxemia characteristically improves with supplemental oxygen (likely due to alleviation of pulmonary vasoconstriction), which differentiates HAPE from other causes of diffuse pulmonary edema. Although potentially fatal, HAPE usually resolves rapidly upon descent to lower altitudes. (Choice B) Acute pulmonary embolism causes dyspnea and hypoxemia; however, jugular venous distension and an absence of pulmonary edema (eg, no ausculatory crackles, clear lungs on chest x-ray) are also expected. (Choice C) Hyperventilation leading to reduced PaCO₂and respiratory alkalosis is expected at high altitude. An extreme drop in PaCO₂ can cause severe alkalosis with associated tingling, numbness, tetany, and possibly seizures, but it does not cause pulmonary edema. (Choice D) Left ventricular function is unaffected in HAPE (the pulmonary edema is noncardiogenic). Myocardial infarction can lead to acute left ventricular dysfunction with pulmonary edema, but it would be expected to present with severe chest pain and to cause jugular venous distension. (Choice E) In response to the reduced PiO₂ at high altitude, the body increases erythrocyte production to increase O₂-carrying capacity. However, this secondary polycythemia does not contribute to pulmonary edema. Educational objective: High-altitude pulmonary edema presents with dyspnea and cough within several days of arrival at high altitude. It is driven by reduced ambient oxygen, which leads to hypoxic pulmonary vasoconstriction and pulmonary arterial hypertension. Individuals with unevenly distributed pulmonary vasoconstriction can develop areas of high capillary perfusion pressure that disrupts the alveolar-capillary membrane, leading to patchy, bilateral pulmonary edema. __________ References: Update on high-altitude pulmonary edema: pathogenesis, prevention, and treatment. (http://www.ncbi.nlm.nih.gov/pubmed/19099331)

A 28-Year-Old Previously Healthy Man Comes to the Urgent Care