Venous gas bubbles in breath hold divers remained a focus of researchers this year, with a notable presentation coming from Danilo Cialoni and his EDAN team1. At EUBS 2017 they presented the extension of study previously reported and described in this blog. After discovering post-dive VGE in one breath hold diver, they studied VGE in 37 elite breath hold divers during their training in 42 meter deep pool with water temperature of 32 oC.
EUBS 2017 has left us with more questions than answers, on the topic of post-dive bubbles.
Ballestra presented the preliminary results of an exploratory study of the effects of sonic vibrations on post-dive venous gas emboli detected by transthoracic echocardiography1. (more…)
Are some divers prone — or resistant — to gas bubbles after diving?
Decompression sickness (DCS), which may occur in divers after decompression from a dive, is dependent on the combined dose of gas saturation during the dive and the rate and magnitude of decompression. However, there is a great variability of outcomes in subjects exposed to the same dive profiles. The variability decreases as the severity of exposure increases.
DCS is correlated with the degree of venous gas emboli (VGE), or “bubbles”, in circulation after a dive. Generally, the higher the VGE grade (more bubbles) the greater the probability of DCS, and vice versa. Similar to DCS, there is a great variance in the probability of VGE appearing postdive. Some researchers who practice VGE detection have hinted that some divers bubble after most dives and may exhibit a high bubble grade (HBG) and others tend not to bubble at all or rarely exhibit HBG. The former are often labeled as bubblers (or high bubblers), while the latter are labeled as nonbubblers (or low bubblers).
Venous gas embolism (VGE), or bubbles, in divers postdive indicates that their decompression was too fast, their bodies became supersaturated and free gas emerged from solution in tissues. The occurrence of free gas is considered a necessary condition for decompression sickness (DCS), which can happen even without VGE. However, the presence of VGE increases the number and types of possible harms to the body and thus the probability of DCS.
A number of studies indicate variability in proneness to DCS among divers; however, the question of whether divers who have suffered DCS produce bubbles more readily in general has not been answered yet. To answer this question, researchers would need to identify “bubblers” and “nonbubblers” and observe the outcomes of their dives over some period of time, which would require a lot of resources and time.
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” (http://jap.physiology.org/content/112/1/91.long), 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.
Post written by: Petar Denoble, MD, D.Sc.