Pathophysiological background of the disease
Pulmonary arterial hypertension is a serious, progressive vasculopathy of the lungs of different aetiologies. Patients experience dyspnea, fatigue, exercise intolerance, syncope and edema. An increased arterial pulmonary pressure is the result of an increased vascular resistance of the pulmonary vessels.
There are five main classifications of both acute and chronic mechanisms that can provoke pulmonary arterial hypertension. One group contains idiopathic and hereditary forms of primary vascular pathologies with normal lung function and basically no cardiopulmonary comorbidities. These patients show only mild to no hypoxia [61]. Other forms of pulmonary arterial hypertension are the result of failure of the left heart, chronic thromboembolic disease or of mixed or unknown origin. Because these disease forms do not originate from the pulmonary system, they are less suitable to be modelled by a human hypoxia platform. This model is better suited for the types of pulmonary arterial hypertension caused primarily by impaired lung functions or hypoxia, like COPD, interstitial lung disease, sleep-disordered breathing, and chronic exposure to high altitude.