Altitude-Induced Pulmonary Hypertension

Excerpt

Mountainous regions are a destination for adventure travel, seasonal work, and permanent residence for many people. More than 40 million people visit high altitude areas (greater than 2500 meters) every year, and a reported 140 million people have a permanent residence at these elevations. The decreased barometric and partial pressures of oxygen at high altitudes can reduce inspired oxygen levels compared to sea level. The body's exaggerated physiological response to rapid ascent, a lower level of inspired oxygen, or the persistent hypoxic stimulus experienced at high altitude can cause significant morbidity and mortality. High altitude associated disease processes can vary from mild to life-threatening. The body's response can present in the form of acute mountain sickness (AMS), high altitude cerebral edema (HACE), high altitude pulmonary edema (HAPE), and ultimately high-altitude pulmonary hypertension (HAPH). AMS develops secondary to rapid ascent and can be described as a "hangover" and include nonspecific symptoms such as headache, nausea, dizziness, fatigue, and insomnia.

HAPE is a progression of acute mountain sickness and presents with acute pulmonary, a complication of the body's poor acclimatization. HACE, the most feared complication of altitude sickness, involves cerebral edema and associated neurological symptoms and sequela. Chronic hypoxic stimuli of high altitude living can result in permanent pulmonary vascular remodeling due to increased pulmonary vascular resistance and define a subgroup of pulmonary hypertension known as HAPH. This article will focus primarily on the pathophysiology, clinical presentation, and management of HAPH.