and circulation bubbles, and between multiple bubbles, for dissolved gas for bubble growth. bubble mechanics equilibrium of forces on the surface is required for a bubble to exist. these are: ambient pressure, exerted on the outside of the surface, acting inwards pressure due to tissue distortion, also on the outside and acting inwards surface tension of the liquid at the interface between the bubble and the surroundings. this is along the surface of the bubble, so the resultant acts towards the centre of curvature. this will tend to squeeze the bubble, and is more severe for small bubbles as it is an inverse function of the radius. the resulting forces must be balanced by the pressure on the inside of the bubble. this is the sum of the partial pressures of the gases inside due to the net diffusion of gas to and from the bubble. the force balance in the bubble may be modified by a layer of surface active molecules which can stabilise a microbubble at a size where surface tension on a clean bubble would cause it to collapse rapidly. this surface layer may vary in permeability, so that if the bubble is compressed it may become impermeable to diffusion at sufficient compression. permeability may vary depending on the specific gas. if the solvent outside the bubble is saturated or unsaturated, the partial pressure will be less than in the bubble, and the surface tension will be increasing the internal pressure in direct proportion to surface curvature, providing a pressure gradient to increase diffusion out of the bubble, effectively "squeezing the gas out of the bubble", and the smaller the bubble the faster it will get squeezed out. a gas bubble can only grow at constant ambient pressure if the surrounding solvent is sufficiently supersaturated to overcome the surface tension or if the surface layer around the bubble provides sufficient reaction to overcome surface tension. clean bubbles that are sufficiently small will collapse due to surface tension if the supersaturation is low. bubbles with semipermeable surfaces will either stabilise at a specific radius depending on the pressure, the composition of the surface layer, and the supersaturation, or continue to grow indefinitely, if larger than the critical radius. bubble nucleation bubble formation occurs in the blood or other tissues. one of the hypothetical loci of bubble nucleation is in crevices in macromolecules, but the actual sites of bubble formation in tissues are not known. a solvent can carry a supersaturated load of gas in solution. whether it will come out of solution in the bulk of the solvent to form bubbles will depend on a number of factors. something which reduces surface tension, or adsorbs gas molecules, or locally reduces solubility of the gas, or causes a local reduction in static pressure in a fluid may result in a bubble nucleation or growth. this may include velocity changes and turbulence in fluids and local tensile loads in solids and semi-solids. lipids and other hydrophobic surfaces may reduce surface tension (blood vessel walls may have this effect). dehydration may reduce gas solubility in a tissue due to higher concentration of other solutes, and less solvent to hold the gas. another theory presumes that microscopic bubble nuclei always exist in aqueous media, including living tissues. these bubble nuclei are spherical gas phases that are small enough to remain in suspension yet strong enough to resist collapse, their stability being provided by an elastic surface layer consisting of surface-active molecules which resists the effect of surface tension. bubble growth once a micro-bubble forms it may continue to grow if the tissues are still supersaturated. as the bubble grows it may distort the surrounding tissue and cause damage to cells and pressure on nerves resulting in pain, or may block a blood vessel, cutting off blood flow and causing hypoxia in the tissues normally perfused by the vessel. if a bubble or an object exists which collects gas molecules, this collection of gas molecules may reach a size where the internal pressure exceeds the combined surface tension and external pressure and the bubble will grow. if the solvent is sufficiently supersaturated, the diffusion of gas into the bubble will exceed the rate at which it diffuses back into solution, and if this excess pressure is greater than the pressure due to surface tension the bubble will continue to grow. when a bubble grows, the surface tension decreases, and the interior pressure drops, allowing gas to diffuse in faster, and diffuse out slower, so the bubble grows or shrinks in a positive feedback situation. the growth rate is reduced as the bubble grows because the surface area increases as the square of the radius, while the volume increases as the cube of the radius. if the external pressure is reduced due to reduced hydrostatic pressure during ascent, the bubble will also grow, and conversely, an increased external pressure will cause the bubble to shrink, but may not cause it to be eliminated entirely if a compression-resistant surface layer exists. the variable permeability model ordering hypothesis states that nuclei are neither created nor totally eliminated during the pressure cycle, and the initial ordering according to size is preserved. therefore, each bubble count is determined by the properties and behaviour of a nominal "critical" nucleus which is at the threshold of bubble-formation – all larger nuclei will form bubbles, and all smaller nuclei will not. bubble distribution decompression bubbles appear to form mostly in the systemic capillaries where the gas concentration is highest, often those feeding the veins draining the active limbs. they do not generally form in the arteries provided that ambient pressure reduction is not too rapid, as arterial blood has recently had the opportunity to release excess gas into the lungs. some of the bubbles carried back to the heart in the veins may be transferred to the systemic circulation via a patent foramen ovale in divers with this septal defect, after which there is a risk of occlusion of capillaries in whichever part of the body they end up in. bubbles are also known to form within other tissues, where they may cause damage leading to symptoms of decompression sickness. this damage is likely to be caused by mechanical deformation and stresses on the cells rather than local hypoxia, which is an assumed mechanism in the case of gas embolism of the capillaries. bubble elimination bubbles which are carried back to the heart in the veins will normally pass into the right side of the heart, and from there they will normally enter the pulmonary circulation and eventually pass through or be trapped in the capillaries of the lungs, which are around the alveoli and very near to the respiratory gas, where the gas will diffuse from the bubbles though the capillary and alveolar walls into the gas in the lung. if the number of lung capillaries blocked by these bubbles is relatively small, the diver will not display symptoms, and no tissue will be damaged (lung tissues are adequately oxygenated by diffusion). the bubbles which are small enough to pass through the lung capillaries may be small enough to be dissolved due to a combination of surface tension and diffusion to a lowered concentration in the surrounding blood, though the varying permeability model nucleation theory implies that most bubbles passing through the pulmonary circulation will lose enough gas to pass through the capillaries and return to the systemic circulation as recycled but stable nuclei. bubbles which form within the tissues must be eliminated in situ by diffusion, which implies a suitable concentration gradient. decompression sickness and injuries main article: decompression sickness intravascular bubbles cause clumping of red blood cells, platelets are used up, white blood cells activated, vascular permeability is increased. the gas in a bubble will equilibrate with the surrounding tissues and will therefore contain water vapor, oxygen, and carbon dioxide, as well as the inert gas. vascular bubbles appear to form at the venous end of capillaries and pass through the veins to the right side of the heart, and thereafter are circulated to the lungs. problems due to vascular decompression bubbles bubbles may be trapped in the lung capillaries, temporarily blocking them. if this is severe, the symptom called "chokes" may occur. if the diver has a patent foramen ovale (pfo)or a pulmonary shunt, bubbles may pass through it and bypass the pulmonary capillaries to enter the arterial blood. if these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. moon and kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological dci or early onset dci is increased in divers with a resting right-to-left shunt through a pfo. there is, at present, no evidence that pfo is related to mild or late onset bends." extravascular bubbles bubbles may form within other tissues as well as the blood vessels. inert gas can diffuse into bubble nuclei between tissues. in this case, the bubbles can distort and permanently damage the tissue. these bubbles may also compress nerves as they grow, causing pain. extravascular or autochthonous bubbles usually form in slow tissues such as joints, tendons and muscle sheaths. direct expansion causes tissue damage, with the release of histamines and their associated affects. biochemical damage may be as important as, or more important than mechanical effects. decompression stress biological stress is a concept developed by hans selye, and can be defined as a "general pathophysiological response, where similar symptoms and signs develop in response to a variety of agents and conditions". this phenomenon is also known as the general adaptation syndrome. decompression is a stressor, and decompression stress is the effect on the organism of the physical and physiological factors associated with decompression. even without any producing acute signs and symptoms, vascular gas bubbles can be an indicator of the magnitude of decompression stress, and as most dives where gas bubbles form only produce minimal symptoms, they may be useful as an indicator of the risk of injury in a particular dive, and therefore could be useful to help develop safer procedures. decompression stress has also been described as the amount of inert gas dissolved in various tissues throughout the body, but this is not meaningful unless compared with the amount that would be stable in those tissues at the current ambient pressure. it is the combined effect of all the factors influencing the formation of inert gas bubbles in the tissues during and after decompression. some of these factors are known and can be measured and quantified, others are known, suspected or hypothetical, but not measurable or quantifiable, and some may still be entirely unknown. decompression stress has been cited as a driver of bubble growth and a risk factor for symptomatic decompression sickness in humans and diving animals. factors influencing decompression stress and risk