A biophysical vascular bubble model for devising decompression procedures

Abstract

Vascular bubble models, which present a realistic biophysical approach, hold great promise for devising suitable diver decompression procedures. Nanobubbles were found to nucleate on a flat hydrophobic surface, expanding to form bubbles after decompression. Such active hydrophobic spots (AHS) were formed from lung surfactants on the luminal aspect of ovine blood vessels. Many of the phenomena observed in these bubbling vessels correlated with those known to occur in diving. On the basis of our previous studies, which proposed a new model for the formation of arterial bubbles, we now suggest the biophysical model presented herein. There are two phases of bubble expansion after decompression. The first is an extended initiation phase, during which nanobubbles are transformed into gas micronuclei and begin to expand. The second, shorter phase is one of simple diffusion-driven growth, the inert gas tension in the blood remaining almost constant during bubble expansion. Detachment of the bubble occurs when its buoyancy exceeds the intermembrane force. Three mechanisms underlying the appearance of arterial bubbles should be considered: patent foramen ovale, intrapulmonary arteriovenous anastomoses, and the evolution of bubbles in the distal arteries with preference for the spinal cord. Other parameters that may be quantified include age, acclimation, distribution of bubble volume, AHS, individual sensitivity, and frequency of bubble formation. We believe that the vascular bubble model we propose adheres more closely to proven physiological processes. Its predictability may therefore be higher than other models, with appropriate adjustments for decompression illness (DCI) data.

Keywords: Active hydrophobic spot; arterial bubbles; bubble expansion; decompression illness.

Figure 1

Frequency of initiation of active hydrophobic spots (AHS). Initiation is defined as the moment the first bubble from an AHS reaches a diameter of 0.1 mm as a function of time from decompression. The dotted line is a suggested smooth function.

Figure 2

Distribution of bubble volume on detachment under pulsatile flow. An exponential function was used to fit the data.

Figure 3

Diagram of specific left arterial blood supply to the brain from the aorta to the anterior cerebral artery. Name of the artery, length (cm), internal diameter (cm), blood flow (mL/sec), and wall thickness (mm) are given from left to right below each. Wall thickness refers to intima‐media thickness (IMT). Because the adventitia is rich in blood supply, it is included with the well‐mixed surrounding tissue. References for sources of the data are provided in the text.

Figure 4

Calculated inert gas tensions (Appendix) along the arterial tree, as depicted in Figure 3, at steady state when gas tension in the surrounding tissue is 500 kPa and in the left ventricle 101 kPa. Values are also calculated for reduction of blood flow in the anterior cerebral artery (A2) to 50%, 20%, and 10%.

Figure 5

Frequency of sheep having various levels of bubble production after decompression. An exponential function was used to fit the data.

Figure 6

Frequency of AHS density on blood vessels.

Figure 7

Frequency of AHS as a function of their productivity: the number of bubbles which became detached within 1 h. Two exponential functions were found which could delineate the frequency.

Figure 8

Time intervals (mean ± SD) between successive detachments from 24 active hydrophobic spots as a function of the detachment sequence. The first interval is the time from the end of decompression to the first detachment. The exponential equation was derived for the 229 data points.