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High-Altitude Pulmonary Hypertension: A Case of Reversal with Descent
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A7006 - High-Altitude Pulmonary Hypertension: A Case of Reversal with Descent
Author Block: B. A. Jalil, K. El-Kersh; Pulmonary, Critical Care, and Sleep Disorders Medicine, University of Louisville, Louisville, KY, United States.
Chronic hypoxemia at high-altitude has been associated with the development of pulmonary hypertension through a variety of mechanisms, though the exact incidence is not known. High altitude pulmonary hypertension is classified as WHO group III. Herein, we present a patient who had echocardiographic evidence of pulmonary hypertension that normalized within a few months of descent from 9000 feet above sea level in Summit County, Colorado to about 500 feet above sea level in Louisville, Kentucky.
An 80-year-old active female with hypothyroidism and previously treated breast cancer presented to our pulmonary hypertension center at the University of Louisville for further evaluation. A few months prior to presentation, she noted worsening exertional dyspnea while on vacation in Colorado after a month long stay at an altitude of about 9000 feet above sea level. She was found to be hypoxic with a resting saturation of 83% on room air. She underwent an extensive work up in Colorado including CT chest, VQ scan, and echocardiogram. Chest computed tomography was unrevealing for parenchymal lung disease or pulmonary emboli and the VQ scan was low probability. Echocardiogram showed flattened interventricular septum, septal bounce, dilated right-ventricular outflow tract, and right-ventricular systolic pressure (RVSP) of 70mmHg. Pulmonary function test showed no obstruction with normal lung volumes. After return to Louisville the hypoxia resolved and repeat echocardiogram showed normalization of right-ventricular overload, return of a normal shaped septum and RVSP estimated at 30mmHg. At 1 year follow up, the patient has not travelled back to elevation and her echocardiogram remains unchanged.
High altitude pulmonary hypertension has been reported in the literature and descent closer to sea level is highly recommended. It is unclear whether descent to sea level carries a prognostic value or a mortality benefit in patients with high-altitude pulmonary hypertension. Those who are not able to descend have been treated with vasodilator therapies, though the literature on this subject is scarce with varying results. It is also important to remember that patients with pre-existing pulmonary hypertension may not tolerate travelling to high altitudes. It is very important to review previous echocardiographic and hemodynamic data with close attention to the elevation at which these tests were performed. In conclusion, our case highlights an unusual cause of pulmonary hypertension with documented reversal upon descent from high altitude.
Author Block: B. A. Jalil, K. El-Kersh; Pulmonary, Critical Care, and Sleep Disorders Medicine, University of Louisville, Louisville, KY, United States.
Chronic hypoxemia at high-altitude has been associated with the development of pulmonary hypertension through a variety of mechanisms, though the exact incidence is not known. High altitude pulmonary hypertension is classified as WHO group III. Herein, we present a patient who had echocardiographic evidence of pulmonary hypertension that normalized within a few months of descent from 9000 feet above sea level in Summit County, Colorado to about 500 feet above sea level in Louisville, Kentucky.
An 80-year-old active female with hypothyroidism and previously treated breast cancer presented to our pulmonary hypertension center at the University of Louisville for further evaluation. A few months prior to presentation, she noted worsening exertional dyspnea while on vacation in Colorado after a month long stay at an altitude of about 9000 feet above sea level. She was found to be hypoxic with a resting saturation of 83% on room air. She underwent an extensive work up in Colorado including CT chest, VQ scan, and echocardiogram. Chest computed tomography was unrevealing for parenchymal lung disease or pulmonary emboli and the VQ scan was low probability. Echocardiogram showed flattened interventricular septum, septal bounce, dilated right-ventricular outflow tract, and right-ventricular systolic pressure (RVSP) of 70mmHg. Pulmonary function test showed no obstruction with normal lung volumes. After return to Louisville the hypoxia resolved and repeat echocardiogram showed normalization of right-ventricular overload, return of a normal shaped septum and RVSP estimated at 30mmHg. At 1 year follow up, the patient has not travelled back to elevation and her echocardiogram remains unchanged.
High altitude pulmonary hypertension has been reported in the literature and descent closer to sea level is highly recommended. It is unclear whether descent to sea level carries a prognostic value or a mortality benefit in patients with high-altitude pulmonary hypertension. Those who are not able to descend have been treated with vasodilator therapies, though the literature on this subject is scarce with varying results. It is also important to remember that patients with pre-existing pulmonary hypertension may not tolerate travelling to high altitudes. It is very important to review previous echocardiographic and hemodynamic data with close attention to the elevation at which these tests were performed. In conclusion, our case highlights an unusual cause of pulmonary hypertension with documented reversal upon descent from high altitude.
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