higbvuyb wrote:
Again, in the context of this argument, long term side effects are irrelevant. Also, you're missing the point, which is that the brain isn't necessary. the 'aid in killing you' part is irrelevant because without a brain, you're going to run out of oxygen and die.
Obviously, running out of oxygen and dying is going to be fatal.
I'm a little confused as well, as to the direction of the argument. From where I sit, and correct me if I'm wrong, the argument is; 1) shooting someone in the heart/center mass
kills them faster/more efficient than a similar shot to the head, thus being more effective means of death. 2) by shooting someone in the heart, the act of stopping the heart and/or bleeding out the person from massive arterial damage, provides brain death quicker than brain death from tissue damage in the brain. 3) damage to the brain with increased intracranial pressure that incapacitates a person and later dies is less efficient than bleeding them out with lack of blood pressure with torso gun shot wounds.
As far as hemorhaging is not inflammation, you are correct; however, as to cranial edema and inflammation due add to ICP that leads to displacement of tissue, short of quoting a pathophysiology book, I'm not sure how to 'prove' that. Google fu?
http://bja.oxfordjournals.org/cgi/conte ... act/99/1/4
Pathophysiology of traumatic brain injury
C. Werner* and K. Engelhard
Klinik für Anästhesiologie, der Johannes Gutenberg-Universität Mainz, Langenbeckstrasse 1, D-55131 Mainz, Germany
* Corresponding author. E-mail:
werner@anaesthesie.klinik.uni-mainz.de
The knowledge of the pathophysiology after traumatic head injury is necessary for adequate and patient-oriented treatment. As the primary insult, which represents the direct mechanical damage, cannot be therapeutically influenced, target of the treatment is the limitation of the secondary damage (delayed non-mechanical damage). It is influenced by changes in cerebral blood flow (hypo- and hyperperfusion), impairment of cerebrovascular autoregulation, cerebral metabolic dysfunction and inadequate cerebral oxygenation.
Furthermore, excitotoxic cell damage and inflammation may lead to apoptotic and necrotic cell death. Understanding the multidimensional cascade of secondary brain injury offers differentiated therapeutic options.
Bolding mine.
Interesting article about viticms of bomb blasts who suffer brain inflammation without physical blunt force trauma to the head.
Another article that studies the inflammation effect in trauma patients. Interestingly enough, the study they points to mitochondria released into the blood stream from dead cells from trauma as the genesis of the immune response.
Anyway, long story short; will bleeding out be a faster death than whacked in the head and 20 minutes to an hour later having swelling in your head squish your brain into unconsciousness? Sure. I concede that if that is the argument. If the argument is, though, that if you shoot person A in the heart and person B in the head, person A drops to the ground and dies while person B keeps fighting like Rambo for two more hours before he lapses into a comma and dies, is stupidity at it's highest. Each senario is rather simplistic; however, and don't take into account many factors. Just having head trauma enough to increase ICP means you've already disrupted the brain tissue causing primary damage, the secondary damage from the swelling comes later. It also matters what you've damaged in the brain, and everyone here is talking like just the cerebrum is getting hit, and not something like the brain stem (which would bring a quicker death than the heart) or cerebellum, or some other structure.
Edit last few sentences, wanted to hit preview and hit submit instead.