To start, the chest cavity will hold all of the blood volume if empty, but in the first moments post GSW those areas are occupied. The vent allows the blood to flow at much lower back-pressure. The second vent decreases back-pressure significantly more than the first hole for a number of reasons; first, the exit is usually larger, second, the tissue has been pulled toward the exit by the passing bullet and the tissue seldom completely plugs the wound as frequently happens on the entry wound, third, the minor increase in blood loss volume effect vs BP reduction is not linear, fourth, the argument is not about absolute death (yes/no) but rather the speed of exsanguination to the point of incapacitance.
I, in agreement with many learned sources, disagree with the offhand dismissal of the value of exit wounds. I do agree absolutely it is a complex equation.
Thanks for your comments. It's always best to discuss these things as gentlemen!
My dismissal of the "value" of exit wounds is not offhand, I assure you. It is based on sound medical and physiological principles. The simplest way to consider it is this: when I have a patient in my ER with a thoracic GSW,
the first thing I do after stabilizing his airway is to put a second (or third, or fourth) hole in his chest. This procedure is called a tube thoracostomy, or chest tube placement in plain English. This can be considered the equivalent of an exit wound, in terms of what it does in the immediate post-injury period. We do this to get blood (and air) out of the chest, because leaving blood and air in there is a significant threat to life.
Free fluid (blood) in the thoracic space is always a bad thing. Unlike air, which can be compressed readily, blood does not compress. Thus bleeding that is contained inside the chest necessarily compresses the lungs and may compress the heart. Both conditions lead to rapid decline in function of these organs and the body. The trivial internal pressure of the lungs is easily and rapidly defeated by even venous blood pressure (5-10 mm Hg), let alone pulmonary arterial pressure (30-40 mmHg) or aortic arterial pressure (>100 mmHg, and higher under stress).
So the notion that internal bleeding is somehow diminished without a free-flowing exit wound, while appealing on an intuitive basis, has no basis in physiology. If it were otherwise, we would be binding up GSW patients rather than opening them up!
Now, a cervid with an abdominal wound may be prone to more rapid exsanguination if there is a large exit wound... but in my experience in both the hunting field and the trauma room suggests that external bleeding from abdominal wounds is much less of a concern than internal bleeding, especially if the liver spleen, abdominal aorta, or major pelvic blood vessels are ruptured. Death from internal bleeding occurs with tremendous speed with any of these injuries. The "gutshot" animal that lives in terrible pain for a day after its shooting is shot in the guts, not these critical organs.
The constant use of the "all failures to exit are bullet failures" eliminates the context when those statements were made.
Good point, and I did not mean to trivialize the point or the context. I can think of several instances where an exit wound should considerably hasten the recipient's demise. A wound to the arterial structures of the hindquarters, for instance... here, the second hole will prevent tamponade within the muscles, and the animal will hemorrhage externally more quickly.
A Cardiac surgeon friend and I just spoke about this and he still completely discounts the concept of cardiac contraction stage influencing distant CNS effect as we believe you hinted at. One over radius squared eliminates that...
Let me put that inference of yours firmly in the garbage can where you and I and your CT surgeon buddy all know it belongs! I did not imply or "hint" that there is any remote CNS effect from thoracic trauma; that particular internet legend was propagated by a fake PhD named Michael Courtney a number of years ago, and there has been ample peer-reviewed research published to thoroughly debunk it.
What I was referring to, rather, was the idea that if a bullet penetrates a ventricle when it is full of blood (end-diastole) it may be more prone to rupture than it would be when it is at its lowest volume (end-systole). At end-diastole, the ventricle is at its upper limit of elasticity, being stretched to capacity; the kinetic energy of the bullet is transferred to the fluid blood inside the ventricle and there is less elastic capacitance of the ventricular wall to absorb that energy without rupturing. I have demonstrated this with post-mortem sheep hearts, but this is of course not the same thing as a living heart; this is my reason for suggesting further research is needed.
My hypothesis is that if a bullet strikes the ventricle at end-systole, the elasticity of the myocardium allows it to stretch and all you get is a bullet-diameter hole. A ventricle with a bullet-diameter hole in it can still pump blood quite effectively, as the larger outflow tract of the aortic/pulmonic valve offers less resistance to blood flow. However, if the bullet hits at end-diastole, the transfer of energy into the fluid contents of the ventricle produces a dramatically larger exit rupture, which offers less resistance than the valve, and as such forward blood flow into the vasculature will all but cease.
In other words, my hypothesis is that a bullet strike when the heart is fully engorged with blood is more likely to cause a catastrophic and near-immediate loss of blood pressure than if the strike occurs when the heart is fully contracted.
