Hypoxic pulmonary vasoconstriction

Hypoxic pulmonary vasoconstriction is a paradoxical, physiological phenomenon in which pulmonary arteries constrict in the presence of hypoxia (low oxygen levels) without hypercapnia (high carbon dioxide levels), redirecting blood flow to alveoli with a higher oxygen content.

The process might at first seem illogical, as low oxygen levels should theoretically lead to increased blood flow to the lungs to receive increased gaseous exchange. However, it is explained by the fact that constriction leads to redistribution of bloodflow to better-ventilated areas of the lung, which increases the total area involved in gaseous exchange.

This improves ventilation/perfusion ratio and arterial oxygenation, but is less helpful in the case of long-term whole-body hypoxia. This is seen in COPD, at altitude and in heart failure.

Several factors inhibit this process including increased cardiac output, hypocapnia, hypothermia, acidosis/alkalosis, increased pulmonary vascular resistance, inhaled anesthetics, calcium channel blockers, PEEP, HFV, isoproterenol, nitrous oxide, and vasodilators.

High altitude pulmonary edema

Main article: High altitude pulmonary edema

Climbing tall mountains can induce full lung hypoxia due to decreased atmospheric pressure. This hypoxia causes hypoxic vasoconstriction that ultimately leads to high altitude pulmonary edema (HAPE). For this reason, most climbers carry supplemental oxygen to prevent hypoxia, edema, and HAPE. The standard drug treatment of dexamethasone does not alter the hypoxia or the consequent vasoconstriction, but stimulates fluid reabsorption in the lungs to reverse the edema.

External links

• American Thoracic Society
• American Journal of Physiology, Lung Cellular and Molecular Physiology
• Overview at ccmtutorials.com