Cardiopulmonary responses at high altitude (HA) and acclimatisation have been studied in great detail; however, the pathophysiology of HA maladies like acute mountain sickness (AMS), high altitude pulmonary oedema (HAPO), HA cerebral oedema (HACO) and thromboembolic disorders is not clear. Rapid induction of healthy individuals to the same altitude (3500 m) produces heterogeneous symptoms as a majority suffer from AMS while a few suffer from HAPO and HACO which could be fatal if not treated promptly. This chapter explains how modulation of various cardiopulmonary responses at HA can lead to the development of hypoxia susceptibility and the occurrence of HA maladies which are primarily vascular. Previous studies, including ours, have shown that hypoxia susceptibility is associated with endothelium dysfunction and vascular remodelling, leading to reduced vascular compliance during hypoxia. B-type natriuretic peptide (BNP) is a known marker of heart failure but also indicates endothelial dysfunction and vascular remodelling at a lower level. Predicting hypoxia susceptibility is important, as the number of inductions to HA is increasing and limited medical facilities are available in difficult terrain. Currently, there is no marker for predicting HA maladies; however, a subclinical elevation of BNP (>15 pg/mL) has been established as a novel marker for predicting HA maladies.