Human pulmonary vascular responses to hypoxia and hypercapnia

Abstract

The ability of alveolar gas composition to influence pulmonary vascular tone has been appreciated for over 50 years. In particular, it has been proposed that both O2 and CO2 could play a role in the matching of perfusion to ventilation within the lung, improving the overall efficiency of gas exchange. A wide variety of experimental approaches has been used to investigate pulmonary vascular effects of the respiratory gases in a range of mammalian species. In this article, we review experiments performed in healthy humans, identify particular difficulties in the interpretation of such experiments, and discuss possible approaches to future study.

BTS guideline for emergency oxygen use in adult patients

“…It is also thought that a high P co 2 can cause pulmonary vasoconstriction, adding to the homeostatic mechanisms of the lung, matching perfusion to ventilation 49 50. As the relationship between P co 2 and carbon dioxide dissolved in the blood is approximately linear over the physiological range (unlike oxygen), blood does not become saturated with carbon dioxide and therefore a high pulmonary venous P co 2 from low V/Q areas can be partially balanced by a low pulmonary venous P co 2 from high V/Q areas.…”

Physiologic responses and plasma endothelin-1 concentrations associated with abrupt cessation of nitric oxide inhalation in isoflurane-anesthetized horses

“…27 This profound response could predispose pigs to a more precipitous decrease in arterial oxygen concentrations secondary to more profound V/Q mismatch. To our knowledge, the HPV response in humans has not been directly compared with that of horses or pigs, but results of research in altitude-induced HPV suggest that there is great variability among individuals, 29,30 which could contribute to the fact that some humans respond to NO inhalation and some do not. This might also explain why some humans develop a rebound effect following cessation of NO inhalation, whereas some develop a gradual decrease in Pao 2 and an increase in Qs/Qt similar to those detected in the horses of the present study.…”

BTS guideline for oxygen use in adults in healthcare and emergency settings

“…It is also thought that a high PCO 2 can cause pulmonary vasoconstriction, adding to the homoeostatic mechanisms of the lung, matching perfusion to ventilation 66 67. As the relationship between PCO 2 and carbon dioxide dissolved in the blood is approximately linear over the physiological range (unlike oxygen), blood does not become saturated with carbon dioxide and therefore a high pulmonary venous PCO 2 from low V/Q areas can be partially balanced by a low pulmonary venous PCO 2 from high V/Q areas.…”