Pulmonary circulation

Abstract

Increased pulmonary vascular resistance (PVR) and pulmonary artery pressure (Ppa) upon ascent to high altitude universally occur in humans and other mammals, although the magnitude can vary almost five-fold among individuals, across species, and with time at altitude from years to many generations. The mechanisms that lead to hypoxic pulmonary hypertension are numerous and have differing contributions to the pressure measured at any one time. The first and best characterized response is acute hypoxic pulmonary vasoconstriction (HPV). Its physiologic relevance or advantage, if any, in healthy humans moving to altitude remains uncertain, but when it is very excessive it can lead within days to high altitude pulmonary edema (HAPE). Sustained very high Ppa over weeks and months can lead to congestive right heart failure of high altitude also known as subacute mountain sickness (SMS) or cor pulmonale or acute right heart failure of high altitude. With longer durations of high pressure in the pulmonary circulation there can be within days sufficient remodelling of the vasculature to protect the pulmonary capillaries, hence avoid HAPE, and within weeks compensatory changes in the right heart to overcome the higher pulmonary vascular resistance and thus avoid SMS. This condition of high altitude pulmonary hypertension (HAPH) is now recognized as a maladaptation to long-term residency at high altitude in some but not all high altitude populations. In this chapter, we will discuss the different aspects of the pulmonary circulation at altitude from the normal physiological response to environmental hypoxia to its contribution to the pathophysiology of high altitude related diseases and review in depth the work of the last decade in these areas.