In the study of terminal ballistics, it is a commonly held belief, established through laboratory testing and actual field/service use, that there is a lower velocity threshold for hydrostatic shock damage in tissue. This velocity threshold is typically held around 2000 to 2200 fps. Hydrostatic shock refers to the pressurized shock wave that travels away from the projectile when it encounters a liquid or semi-liquid solid. While these forces exist at lower velocity impacts, most living tissue is elastic and fairly resistant to these forces under a certain projectile impact velocity. Tissue will be displaced but will stretch and rebound with little or no damage. However, above about 2000 to 2200 fps, we see that these hydrostatic shock forces become too fast and too violent for elasticity of the tissue. The tissue will be stretched beyond its breaking point and will tear, causing potentially massive amounts of damage well beyond the actual trajectory of the projectile. So typically, when dealing with common service handgun rounds like the .45 ACP, energy plays very little role in incapacitation. Rather, all that matters is diameter and penetration, because only the permanent crush cavity, that tissue actually crushed and physically displaced by the projectile, will remain; there is no hydrostatic shock damage. So your wound channel is typically a fraction of an inch in diameter, usually about 80% of the diameter of the projectile when it penetrates, because again, tissue is elastic. At the same time, even a small caliber, high velocity rifle round is capable of doing several orders of magnitude more damage than any service handgun. The high velocity of a rifle round like the 5.56 causes cavitation damage often a couple inches from the trajectory of the round. So even an anemic high velocity rifle round is capable of doing 2 to 3 times the damage of any service caliber round. Obviously, however, we can not speak in absolutes about something for which there are so many variables. Gel testing is one thing, but actual street and field results are quite another. In gel testing, we can see that nose profile, the degree and speed of a projectile's expansion, and other factors are important. In the field, we see that organ density, shot presentation, and the complexity of living bodies makes conjecture dubious and speaking in absolutes foolish. I have seen pictures and heard first hand accounts of large caliber magnum handgun and rifle rounds operating below 2000 fps but still apparently capable of doing some hydrostatic shock damage. Rounds like the .45-70 and the .500 S&W seem to be capable of producing cavitation damage beyond the trajectory of the round, regardless of the fact that they are operating several hundred feet per second below commonly held velocity thresholds. So what role does caliber and nose profile play in the creation of hydrostatic shock? Is there an established relationship between the caliber of a round and what velocity is necessary to create cavitation damage in tissue? To what degree have handgun hunters and those hunting with large bore rifles witnessed this phenomenon?