Decompression sickness (DCS) is a condition that may result from quick decompression, which may occur when diving or flying. One mechanism involved in DCS is the passage of venous gas emboli (VGE or “bubbles”) to the arterial side of circulation; this is known as arterialization.
Until recently, arterialization was considered a rare event except when there is a passage in the heart wall because of a patent foramen ovale, (PFO), atrial septal defect or ventricular septal defect. In people with normal hearts it was previously thought that when venous gas passed through the narrow pulmonary capillaries, the potential for VGE was eliminated. It is known that some pathways allow up to five percent of venous blood to bypass pulmonary capillary filters, but the caliber of these bypasses was considered too small to allow VGE to pass through. Occasionally, some bubbles would arterialize, but it was considered a rare event. Recently, however, several authors have reported postdive VGE arterialization, but the true incidence of this phenomenon was not known.
Our colleagues of University Split, Ljubkovic M., et al. studied VGE arterialization and published two papers. The first, “Determinants of arterial gas embolism after scuba diving”, reports results of laboratory testing and postdive findings. They tested 34 subjects by injecting saline with air bubbles in an arm vein and used echocardiography to monitor for bubble passage to the left side of the heart. In 23 out of 34 subjects, the transpulmonary passage of bubbles was observed at rest or after mild exercise. Nine subjects with confirmed arterialization in lab conditions also experienced arterialization after a field dive. All nine had large amounts of VGE in their right heart (VGE grade of 4B or greater). In subjects with no arterialization in lab conditions, there was no arterialization postdive either despite five of them having VGE grade 4B.
Authors concluded that “Postdive VGE arterialization occurs in subjects that meet two criteria: 1) transpulmonary shunting of contrast bubbles at rest or at mild/moderate exercise and 2) VGE generation after a dive reaches the threshold grade.”
It is important to notice that none of the nine divers with echocardiographically detected arterialization had any symptoms or signs of DCS or cerebral arterial gas embolization (CAGE). There is also no clear evidence concerning long-term consequences of chronic embolization in divers without history of manifested DCS or CAGE. Read the Alert Diver article, “Effects of diving on the brain” to learn more.
The significance of these findings is dubious. In the first place, it is now clear that a certain level of arterialization occurs more often than previously assumed and proven. One of the reasons may be in increased resolution of new generations of echocardiography machines, which enables us to detect smaller VGE than before. Second, it is reasonable to assume that occurrence of DCS in cases of VGE arterialization depends on the size and quantity of VGE, but the threshold values are not known. Third, a loose relationship between the presence of PFO and DCS may be due to not accounting for transpulmonary bubble passage.
Thus, we are looking forward to results of a prospective study conducted by Germonpre, P. and colleagues, which relates to the presence of VGE in carotid artery (accounting for PFO and transpulmonary passage) to DCI.