The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-Induced Hypercapnia During Acute Exacerbations of Chronic Obstructive Pulmonary Disease

BTS guideline for emergency oxygen use in adult patients

“…However, where respiratory mechanics are such that increased ventilation is not possible, Pa co 2 will rise. Several authors have reported that this mechanism is more important than reduction in ventilatory drive in producing hypercapnia when supplementary oxygen is administered, but this continues to be a controversial area of respiratory physiology 98 – 105…”

“…This phenomenon is also seen in normal individuals. Several clinical studies have suggested that “hypoxic drive” makes only a small contribution to the rise in Pa co 2 that is seen clinically when high-dose oxygen is given to patients with COPD, but one recent study has supported this mechanism 98 – 105…”

“…What he actually said in 1967 was as follows: “It is usual to attribute the rise in PaCO2 in these patients to removal of the hypoxic drive to ventilation but I share the doubts of Pain and co-workers103 that this is the whole story; changes in the pulmonary circulation may also be important” 66. Most but not all subsequent studies have shown that Campbell was correct in this assumption 98 – 105. Another curious feature of hypercapnia in acute exacerbations of COPD is that it is not universal 66.…”

Gas exchange and ventilation–perfusion relationships in the lung

“…In other words, for any given CO 2 content, PCO 2 will be higher with greater haemoglobin O 2 saturation. The Haldane effect has been estimated to explain 6-78% of the increase in PaCO 2 in COPD patients after administration of supplemental O 2 [61,65,66]. FIGURE 12 Hypoxic pulmonary vasoconstriction (HPV) occurs in lung regions with low PAO 2 , effectively redistributing blood flow away from the hypoxic regions and towards better oxygenated regions.…”

Oxygen: kill or cure? Prehospital hyperoxia in the COPD patient

“…21 Whilst some studies have questioned the role of hyperoxic respiratory depression as the primary mechanism for hypercapnia, a slight reduction in minute ventilation remains a likely cause of carbon dioxide retention. [22][23][24][25][26][27] Many nonspecialist textbooks have over-emphasised the reduction in ventilation, hypothesising that the patient would become bradypnoeic, hypoxic, and ultimately apnoeic. The effects of hypercapnia and acidosis have been less well-emphasised.…”