Altitude Induced Pulmonary Hypertension

The mountains are popular and sought out destinations for adventure travel, seasonal work, and permanent residence for a growing number of the world's population. More than 40 million people visit areas of high altitude (greater than 2500 meters) every year, and a reported 140 million people have a permanent residence at these elevations. At high altitudes, the concentration of oxygen in inspired air is much lower when compared to sea level due to a decrease in barometric pressure and a decrease in the partial pressure of oxygen. The body's physiological response and adaptation to a hypoxic stimulus such as high altitude can cause significant morbidity and mortality and presents 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). The disease processes can vary from mild to life-threatening. AMS develops due to rapid ascent and can be described as a hangover and includes nonspecific symptoms such as headache, nausea, dizziness, fatigue, and insomnia. HAPE is a progression of the disease process and presents with acute pulmonary complications due to poor acclimatization. HACE, the most feared complication of altitude sickness, involves the development of neurological symptoms and sequela due to cerebral edema. These conditions are essentially a range of severity based on similar pathophysiology resulting from hypoxic stimuli during rapid ascent to high altitudes. 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 activity will focus primarily on the pathophysiology, clinical presentation, and management of HAPH.