In the present study, we found that only seven of 101 patients (6.9 percent) developed more than a 100 mm Hg decrease in PaOg/FIOa during the inflation of PAC balloon; the majority of patients showed a relatively small decrease or increase in Pa02. Neither the decrease in PetC02 nor baseline PAP was correlated with the decrease in Pa02 during PAOP measurements. The maximum decrease in PaOa/FIo2 induced by the balloon inflation was 186 mm Hg in the present series of patients. Such a degree of decrease in Pa02 must be crucial and large enough to deteriorate oxygen delivery to the tissues if it occurs in patients with cardiopulmonary instability or acute respiratory failure, even though CO remained unaffected during PAOP measurements.
Although the phenomenon caused by the balloon inflation is not the same as that of pulmonary embolism, both the balloon and embolus have a tendency to flow to oxygenated, well perfused lung regions and produce mechanical obstruction of pulmonary blood flow to those regions with a concomitant increase in the dead space. Hypoxemia in acute pulmonary embolism is well known as a consistent and important clinical feature, and its severity seems to be dependent on the degree of occlusion of pulmonary vasculature and probably bronchoconstriction due to released chemical mediators. Although the degree of occlusion can be predicted by the magnitude of PaC02-PETC02 difference in pulmonary embolism, our results indicate that the magnitude of the decrease in PetC02 could not be a predictable value for the decrease in PaO£ during PAOP measurements. further
Inflation of the PAC balloon could affect pulmonary oxygenation in at least four ways: by mechanical obstruction of pulmonary blood flow, by neuronal response of pulmonary vasculature, by local changes of existing humoral mediators and thus, probably, by changes in bronchial motor tone. All of these could cause redistribution of pulmonary blood flow within the lungs. The mechanical obstruction of the major pulmonary artery due to the balloon has been considered a main cause for a remarkable decrease in Pa02 in patients with reduced pulmonary vasculature. Lung size as assessed by total lung capacity and airway area are significantly smaller in female compared with male adults, even in the subjects matched for height. It is thus possible that smaller lung capacity in females could be responsible for enhancing the ventilation-to-perfusion mismatching during the balloon obstruction and thus for the decrease in Pa02. The balloon inflation might also induce neuronal responses such as reflex pulmonary vasoconstriction and hypocapnic bronchial constriction, and pulmonary vascular responses to hypoxia; and vasoactive substances are different between male and female animals. Therefore, although no report on gender difference exists in human pulmonary vasoreactivity, we cannot exclude the possibility that neuronal as well as humoral factors might be responsible, to some extent, for the present results. Further, other factors affecting pulmonary vasculature and vasoreactivity, such as cigarette smoking as well as a patients age, must be taken into account for the present results.