Mechanisms of hypoxemia

Abstract

A fundamental aspect of cardiopulmonary homeostasis is the adequate delivery of oxygen to meet the metabolic demands of the body. Cardiac output, O2-carrying capacity (i.e., hemoglobin concentration and quality), and arterial PO2 (PaO2) determine O2 transport. Relevant to this discussion, arterial hypoxemia commonly occurs in patients with acute respiratory failure (ARF). If arterial hypoxemia is severe enough, it is not compatible with life. The two primary causes of ARF are acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and chronic obstructive lung disease (COPD). Although the treatment for arterial hypoxemia always includes increases in the fractional inspired O2 concentration (FIO2), the degree to which patients’ PaO2 improves and the need for adjuvant therapies differ markedly between these two groups of disease processes. The mechanisms by which arterial hypoxemia occurs in ALI/ARDS and COPD have been characterized using the multiple inert gas elimination technique (MIGET) approach [1]. MIGET provides precise estimates of the distributions of alveolar ventilation and pulmonary perfusion (VA/Q) and their relationships, there is no need to change the FIO2 during measurements, hence avoiding variations in the pulmonary vascular tone, and it facilitates the unraveling of the active interplay between intrapulmonary, namely VA/Q imbalance, intrapulmonary shunt and limitation of alveolar to end-capillary O2 diffusion, and extrapulmonary (i.e., FIO2, total ventilation, cardiac output and oxygen consumption) factors governing hypoxemia [2].