.40 Caliber Pressure Wave Effects

[Shear_stress]

pressure wave radiates outward nearly equally in all directions for most bullet designs

Hi Michael.

A pressure wave will radiate equally in all directions like a ripple in a pond, but this does not mean a hydrostatic condition. Also, the factors that affect the intensity of the pressure wave (bullet velocity and geometry, for example) change constantly as the bullet slows down and deforms. Add to this the nonlinear properties of human tissue, and you've got a doozy of a problem to solve.

 

[Michael Courtney]

Double post, sorry.

 

[Michael Courtney]

Hi Michael.

A pressure wave will radiate equally in all directions like a ripple in a pond, but this does not mean a hydrostatic condition. Also, the factors that affect the intensity of the pressure wave (bullet velocity and geometry, for example) change constantly as the bullet slows down and deforms. Add to this the nonlinear properties of human tissue, and you've got a doozy of a problem to solve.

The technical details do get tricky at this level of analysis. I appreciate your suggestions. We should consider calling the effect a "stress wave" rather than a pressure wave.

Fortunately, the main point of the stress/pressure wave is that the effects of a bullet can be transmitted beyond the reach of the stretch and crush cavities, and this can be seen on the phenomenological side without developing a finite element model from the ground up.

Thanks,

Michael Courtney

 

[RyanM]

So you're referring to a pressure wave that is caused by the temporary cavity, rather than the sonic pressure wave? That's completely different, and may indeed be a significant source of ballistic trauma in some cases, though the vast majority of handgun cartridges do not cause a very substatial temporary cavity.

I can give you my equation, but unfortunately I cannot make available all the necessary equations to calculate the temporary cavity, until and unless I get word back from Duncan MacPherson about whether he would mind me distributing a spreadsheet calculator which makes use of his equations.

[ impact velocity (fps) / cavitation threshold velocity (fps) ]^2 * bullet weight (grains) / 37.85 (constant) - permanent cavity volume

If the impact velocity is between the cavitation threshold and 2 * cavitation threshold, multiply the result by

velocity / cavitation threshold - 1

If velocity is under the cavitation threshold, there is no temporary cavity beyond the diameter of the bullet. If it's over 2 * threshold, use the first equation unmodified.

That set of equations gives you the volume of the temporary cavity in cubic inches. The cavitation threshold velocity must be determined using one of Mr. MacPherson's equations. It's around 400-700 for most bullets.

To determine the diameter of the temporary cavity at the widest point, the most accurate method I've found (which is not overly complex) is

2 * sqrt[ temporary cavity volume (in^3) * 3 + permanent cavity volume (in^3) / pi / penetration depth (in) ]

Permanent cavity volume and penetration depth in my spreadsheet are both also derived from MacPherson's equations. This equation assumes the volume of the temporary and permanent cavities is in the form of a cone, and gives you the diameter of the base of the cone. It's not 100% accurate, but it's "good enough for government work."

The permanent stretch equation is much easier. If the temporary cavity is under 8", it's

0.5 * temporary cavity max diameter - 0.5

If it's over 8", then

1.45 * temporary cavity max diameter - 8.1

Whichever equation you use, if the impact velocity is under 2,500 fps, multiply the result by

striking velocity / 2,500

If striking velocity is over 2,500, just use that result. This assumes that the projectile does not fragment.

If it does fragment, then add the results of this second equation. I am much less certain of the accuracy of this one, however. In this case, fragmentation means the "normal" type of fragmentation which high-powered rifle softpoints produce; a main bullet mass and many, many, tiny fragments.

0.02961687062 * fragmentation percent (integer; i.e. 30% = 30.0) + 0.0000702724359 * fragmentation percent^2 - 0.00001961028555 * fragmentation percent^3 + 0.0000002693036131 * fragmentation percent^4 - 0.000000001073717949 * fragmentation percent^5 * (0.00025 * striking velocity - 0.25) * temporary cavity diameter

If striking velocity is under 1,000 fps, then assume that there is no extra tearing at all due to the perforation of tissues.

As examples, here are the results for a few bullets:

150 grain .308 striking at 2500 fps, expanding to 0.60", with 20% fragmentation:
penetration, 15.3"
volume of tissue crushed, 3.2 in^3
avg. diameter crushed, 0.55"
max temporary cavity, 5.4"
max permanent cavity, 3.8" (in muscle, more in lungs)

The exact same bullet with no fragmentation produces:

penetration, 18.6"
volume of tissue crushed, 4.0 in^3
avg. diameter crushed, 0.55"
max temporary cavity, 5.5"
max permanent cavity, 2.8" (in muscle, more in lungs)

9mm 124 grain hollowpoint striking at 1100 fps, expanding to 0.55"

penetration, 13.3"
volume of tissue crushed, 2.4 in^3
avg. diameter crushed, 0.52"
max temporary cavity, 2.5"
max permanent cavity, 0.57" (in muscle, more in lungs)

edit: mistake in an equation

 

[ghost squire]

I'll be sure to report back here if our estimate of the impact velocity needs to be revised.

Excellent, and I for one would like to thank you for your work.

 

[benEzra]

Very interesting work, sir. Thank you for sharing it.

 

[Michael Courtney]

So you're referring to a pressure wave that is caused by the temporary cavity, rather than the sonic pressure wave? That's completely different, and may indeed be a significant source of ballistic trauma in some cases, though the vast majority of handgun cartridges do not cause a very substatial temporary cavity.

By "pressure wave" I mean everything a high-speed pressure gauge would measure. One can insert a high-speed PZT-based or strain-based pressure gauge into ballistic gelatin and measure this pressure wave. The pressure wave includes the sonic pressure wave, but has different components as well.

So you're referring to a pressure wave that is caused by the temporary cavity, rather than the sonic pressure wave?

I would tend to consider the TSC an effect rather than a cause of the pressure wave. Pushing tissue aside requires a force, and a force applied over an area is a pressure. If there were no pressure, there would be no force, and the tissue would not be moved from it's initial static (rest) condition. Of course, once the tissue reaches its maximum displacement, the elastic force restores the tissue which increases the duration of the pressure wave as it bounces around, so in some sense the TSC contributes because the elasticity of the stretched tissue provides a restoring force.

The volume of the TSC is highly correlated with the peak pressure magnitude, so there is a very close relationship.

In experiments using 10-20 lb mammals immersed in water, we were able to incapacitate the test subject with near misses fired into the water 1-2" from the chest and neck area of the test subject. The idea was to transmit a pressure wave from the water to the chest and neck area of the test subject without a temporary stretch cavity or a permanent crush cavity even being present.

We have an experiment on the drawing board to apply a pressure wave into a goat/deer/sheep-sized test subject via a cannula connecting an external saline filled bladder to the carotid or femoral artery. Shooting the saline bladder would transmit a pressure wave into the artery. There are some technical challenges we are working through.

We have another experiment on the drawing board to shoot test subjects with two bullets nearly simultaneously and study how wounding and incapacitation vary with a small delay between the bullet impacts. Since the pressure wave of the two bullets will add by the principle of superposition, observing how this enhances the wounding and incapacitation effects should suggest whether it is the early (sonic and shock) or later (TSC-related) components of the pressure wave making the greater contribution. In other words, the idea is to study wounding (volume of destroyed tissue, volume of moderate to severe hemorrhaging) and incapacitation (average distance run after the shot in deer, or average incapacitation time in goats, pigs, or sheep) vary as the delay between the bullets is varied from zero to 100 ms.

At zero delay, we expect maximum superposition of the pressure waves. This should lead to an estimated wounding enhancement of 40% (compared to 100 ms delay) and an estimated incapacitation enhancement of 20% (compared to 100 ms delay). As the delay between bullet impact is increased from 0 ms to 100 ms, the wounding/incapacitation enhancement should decrease. The delay values where the wounding/incapacitation enhancement shows a sudden drop suggests the more important component of the pressure wave. If the enhancement drops markedly within the first 10 ms, this suggests the sonic and leading shock wave play an important role, because the TSC-related wave follows later. If the enhancement does not drop markedly until longer delay times, this suggests that either the sonic and leading shock wave have a longer than expected reverberation time, or that the TSC-related wave plays the more important role.

Both of these future experiments are considerably more expensive than the work we have done to date, and carrying them out will require acquisition of adaquate funding.

Michael Courtney

 

[Michael Courtney]

I can give you my equation . . .

Thank you very much.

Michael Courtney

 

[Shear_stress]

Hi Michael,

Please clarify the following:

In experiments using 10-20 lb mammals immersed in water, we were able to incapacitate the test subject with near misses fired into the water 1-2" from the chest and neck area of the test subject. The idea was to transmit a pressure wave from the water to the chest and neck area of the test subject without a temporary stretch cavity or a permanent crush cavity even being present.

First, how exactly did you carry out this experiment? How did you determine if the 10-20 lb mammal was incapacitated? Are you sure it wasn't just because you were holding an air-breathing animal underwater?

Second, how would the results of this experiment be applicable to a study of internal wounding on humans?

It would be easier if you could just tell us where we can find a copy of the journal article.

Thanks!

 

[Shawn Dodson]

Dr. Courtney writes:

It was my impression that the IWBA idea is that the bullet has to physically impact the tissue to cause damage, so the damage is limited to the actual diameter of the bullet at that point in the wound tract.

Untrue. The temporary cavity is known to damage tissues, even resilient ones, when the strain placed upon them stresses the tissues beyond their elastic limits.

Correct me if I am wrong, but doesn't _Handgun Wounding Factors and Effectiveness_ say…

So we’re not mixing apples & oranges, let me clarify that HWFE is not an “IWBA” document.

So, the IWBA viewpoint seems to be that the only way for a handgun bullet to damage tissue is to crush it by direct contact. Thus, the diameter of the permanent cavity cannot exceed the diameter of the bullet as it passes a given point along the wound channel. If the maximum diameter of the bullet exceeds the final recovered diameter because the bullet erodes a bit, then the permanent cavity diameter can also decrease. But this isn't a very large difference, and if I recall correctly, it is a common and accepted practice for JHP handgun bullets to estimate the permanent cavity volume as the recovered frontal area of the bullet times the penetration depth.

The IWBA viewpoint includes the concept of “reliable,” as in “reliable tissue damage.”

You describe the entry wound as, “pulverized a large (1.5” diameter) on the inside of the rib cage and in the liver….” I wouldn’t be surprised if the bullet had expanded 180-200% (.72 - .80 caliber) at this point along the wound track. It probably was also beginning to shed fragments.

The increased damage I observe on the exit (interior) side of the thoracic wall, as shown in your photo, is consistent with permanent disruption caused by the temporary cavity. As the bullet penetrated the wall of the thorax it expanded in the musculature between the ribs. The ability of the rib muscle to stretch was limited by its relatively short length as well as being attached to rib bones. In essence the wounding effect of the temporary cavity produced a sort of cone-like “beveled” wound in the wall of the thorax – the entrance wound was small and the exit wound (on the inside of the rib cage) was substantially larger in diameter because it could not tolerate stretching. In effect, the wound track through the rib muscle was short and the exit side was burst open by the temporary cavity.

Indeed, all the increased damage you observed is caused by the temporary cavity. The tissues are located along the wound track where the diameter of the temporary cavity is greatest.

If one stops to consider that the temporary cavity is, in essence, blunt force trauma delivered at 1/10th bullet velocity, then might be able to imagine the amount of violent force involved.

As velocity decreases with penetration soft tissues have time to move out of the bullet’s way – instead of being crushed by the oncoming bullet the tissues have time to stretch around the bullet as it passes through. This decreases the diameter of the permanent cavity. Thus the “effective permanent cavity” is larger in diameter at the beginning of the wound track.

It is common *FBI practice* to estimate permanent cavity volume in the manner you describe, for comparative purposes. Fackler may have done it at one time, although off the top of my head I’m unaware that he ever did. To the best of my knowledge, Fackler/IWBA have never been concerned about the *volume* of the permanent cavity – just how deep and how big?

I picked up the term "Permanent Crush Cavity" at the Firearmstactical.com web site.

Indeed you did. In the context of shotgun pellets, spherical shot, propelled at typical shotgun velocities, produce a crush injury.

Let me apologize, however, for using the term “permanent wound” in my earlier post when I should have said “permanent disruption.” Permanent disruption includes damage produced in soft tissues by the temporary cavity.

Here are terms I use and what they mean (my understanding has evolved and matured with time, so I won’t be surprised if you find past inconsistencies):

Permanent cavity – the hole crushed by the bullet.
Temporary cavity – the tissues that are violently shoved aside by the passing bullet.
Permanent disruption – all permanent tissue damage caused by permanent cavity, temporary cavity and fragmentation.

This seems to contradict the excerpt from _Handgun Wounding Factors and Effectiveness_ quoted above.

HWFE also states: “All handgun wounds will combine the components of penetration, permanent cavity, and temporary cavity to a greater or lesser degree.” Therefore, the effects vary due to the characteristics of the particular projectile when it hits, as well as the characteristics of the tissues involved and their location along the wound track in relation to the wounding components.

Once again, I found the term [temporary stretch cavity] in use at the Firearmstactical.com web site.

The cited documents are a product of the former U.S. Immigration and Naturalization Service, which are somewhat verbose.

Any time there is a dynamic force applied to a viscous or visco-elastic medium, a pressure wave is created. From a physics viewpoint, this is the pressure supplying the force which expands and decelerates the bullet.
……….
A more visual (but less scientific) manner to view the pressure wave is to view it's effect when shooting fruit. In short, when you shoot a watermelon, it explodes due to the outward force of the pressure wave.

The explosive effect is produced by the temporary cavity; therefore your “pressure wave” is, in fact, the temporary cavity, which follows in the wake of the passing bullet.

 

[Shawn Dodson]

Dr. Courtney writes:

Pushing tissue aside requires a force...

Indeed, inertial force.

 

[Shear_stress]

Shawn,

Considering Michael's shifting terminology, his incomplete grasp of continuum mechanics (which is a cornerstone of biomechanics), and his references to unpublished studies of dubious experimental value, I am not convinced he is the real deal.

 

[Michael Courtney]

Shawn,

Considering Michael's shifting terminology, his incomplete grasp of continuum mechanics (which is a cornerstone of biomechanics), and his references to unpublished studies of dubious experimental value, I am not convinced he is the real deal.

I freely admit that I am not the Biomechanics expert in our research group. We have a scientist with a PhD in Biomechanical Engineering from Harvard University on our team who grasps certain issues more completely than I do.

My PhD is in Physics (from MIT), and my areas of specialty are wave propagation, statistics, and pressure measurement.

Here is a list of my publications:

Michael Courtney and Daniel Kleppner, Physical Review A 53, 178 (1996)

Michael Courtney, Chaos 6, 1 (1996).

Michael Courtney, Physical Review A 51, 4558 (1995).

John A. Shaw, John B. Delos, Michael Courtney and Daniel Kleppner, Physical Review A 52, 3695 (1995).

Michael Courtney, Hong Jiao, Neal Spellmeyer, Daniel Kleppner, Jing Gao and J.B. Delos, Physical Review Letters 27, 1538 (1995)

Michael Courtney, Hong Jiao, Neal Spellmeyer and Daniel Kleppner, in the proceedings of the 4th Drexel Symposium on Quantum Nonintegrability (1995).

Michael Courtney, Neal Spellmeyer, Hong Jiao and Daniel Kleppner, Physical Review A 51, 3604 (1995).

Michael Courtney, Hong Jiao, Neal Spellmeyer and Daniel Kleppner, Physical Review Letters 73, 1340 (1994)

B.D. Simons, A. Hashimoto, M. Courtney, D. Kleppner and B.L. Altshuler, Physical Review Letters 71, 2899 (1993)

G. Chanmugam, P.E. Barrett, Kinwah Wu and M.W. Courtney, Astrophysical Journal Supplement Series 71, 323 (1989)

L.F. DiMauro, Dalwoo Kim, M.W. Courtney and M. Anselment, Physical Review A 38, 2338 (1988)

Michael Courtney

 

[Michael Courtney]

Hi Michael,

First, how exactly did you carry out this experiment? How did you determine if the 10-20 lb mammal was incapacitated? Are you sure it wasn't just because you were holding an air-breathing animal underwater?

After the shot, the mesh confining the test subject was removed, and the animal was determined to be incapacitated if it failed to run a distance of 20' in one minute. Some of the test subjects were killed instantly, and there were no determinations of incapacitation that were even close. Either the test subject was completely immobile or barely able to move, or it was off to the faces and past 20' in under 5 seconds.

The test subjects were confined in such a way that they could breath by holding their heads out of the water. We are also certain that other aspects of our experimental design wer not causing incapacitation because the 147 grain 9mm WWB load repeatedly failed to cause incapacitation in numerous attempts. This load creates a much smaller pressure wave than the other loads we tested that produced incapacitation.

Second, how would the results of this experiment be applicable to a study of internal wounding on humans?

We're not adherents to the presupposition that incapacitation can only occur by wounding that is easily detectable to a trauma surgeon or medical examiner. Our goal in this experimental design was to see if a ballistic pressure wave could incapacitate mammals without any wound channel present. This idea is important when considering whether humans might experience incapacitation via effects of the pressure wave acting beyond the wound channel. It's not proof, of course, but the demonstration of a biological effect in live animals of this side is useful for indicating that humans probably experience a similar effect.

It would be easier if you could just tell us where we can find a copy of the journal article.
Thanks!

A report is currently in preparation for publication. This experiment is described along with the results of two related projects. We are limited by a non-disclosure agreement not to distribute pre-publication copies, but we can email or post the current copy of the abstract.

Michael Courtney

 

[Shear_stress]

The most recent publication date you list is from 1996 and the subjects of these papers seem to be biased toward particle or quantum physics.

A report is currently in preparation for publication. This experiment is described along with the results of two related projects. We are limited by a non-disclosure agreement not to distribute pre-publication copies, but we can email or post the current copy of the abstract.

Well, if your group is as capable as you say, it should have a list of recent publications that you can reference. Also, what is the name of your research group? Where is it located? Also, please post the website of your research group. A Google search turns up nothing.

Michael Courtney may exist, but that doesn't mean you are him.

 

[Michael Courtney]

Untrue. The temporary cavity is known to damage tissues, even resilient ones, when the strain placed upon them stresses the tissues beyond their elastic limits.

Thanks for taking the time and effort to answer.

I had been under the impression that the IWBA position was that this only occurs for rifle bullets, and I believe I've read in multiple Fackler publications that the temporary cavity is not a reliable source of wounding via handgun bullets. It seems that there has been an evolution in understanding. Thanks for helping bring me up to date.

So we’re not mixing apples & oranges, let me clarify that HWFE is not an “IWBA” document.

Thanks. I guess I was considering most of the stuff favorably referenced on the firearmstactical web site to represent IWBA viewpoints.

You describe the entry wound as, “pulverized a large (1.5” diameter) on the inside of the rib cage and in the liver….” I wouldn’t be surprised if the bullet had expanded 180-200% (.72 - .80 caliber) at this point along the wound track. It probably was also beginning to shed fragments.

That is my thinking also.

Indeed, all the increased damage you observed is caused by the temporary cavity. The tissues are located along the wound track where the diameter of the temporary cavity is greatest.

I agree that one cannot ascribe the pulverized tissue to the pressure wave independently of the temporary cavity because they occur in the same region. However, we do observe less severe wounding in areas seemly beyond the reach of the temporary cavity, specifically the minor hemorrhaging of the muscle tissues on the abdominal wall and rib cage opposite the entrance wound and the more severe hemorrhaging around the entry wound (aka bloodshot meat).

We've also seen major hemorrhaging in unborn fetuses of does shot broadside through the center of the chest with the 125 grain Triton Quik-shok at 1450 FPS. This is far beyond the reach of the temporary cavity. We've never seen this hemorrhaging with low pressure wave projectiles. We believe that the pressure wave that originates at the center of the chest is focussed by the approximately ellipsoidal shape of the thoracic cavity and hits the fetus pretty hard.

If one stops to consider that the temporary cavity is, in essence, blunt force trauma delivered at 1/10th bullet velocity, then might be able to imagine the amount of violent force involved.

Sure, but the pressure wave delivers blunt force trauma also, and it can deliver it beyond the reach of the temporary cavity.

Here are terms I use and what they mean (my understanding has evolved and matured with time, so I won’t be surprised if you find past inconsistencies):

Permanent cavity – the hole crushed by the bullet.
Temporary cavity – the tissues that are violently shoved aside by the passing bullet.
Permanent disruption – all permanent tissue damage caused by permanent cavity, temporary cavity and fragmentation.

Thanks for taking the time to explain. My understanding is evolving to, and I am grateful for your assistance in this process.

The explosive effect is produced by the temporary cavity; therefore your “pressure wave” is, in fact, the temporary cavity, which follows in the wake of the passing bullet.

As I wrote before, the temporary cavity is the tissue response to an applied force via the pressure wave. The leading edge of the pressure wave has passed, and the movement of the tissue follows. The volume of the temporary cavity is thus highly correlated with the magnitude of the pressure wave. However, the pressure wave extends well beyond the reach of the temporary cavity, as described above. We believe this has important consequences for both wounding and incapacitation.

Michael Courtney

 

[Michael Courtney]

Well, if your group is as capable as you say, it should have a list of recent publications that you can reference. Also, what is the name of your research group? Where is it located? Also, please post the website of your research group. A Google search turns up nothing.

A significant part of science is public disclosure.

The Ballistic Testing Group has been active since 2001. The abstract I mentioned is for our first publication which is in preparation. We are under a non-disclosure agreement which prevents release of a certain other information prior to publication. One motive for retaining a degree of privacy at this point is to minimize interference from animal rights activists. We believe that after certain information is disclosed we will encounter a much larger rate of interference by animal rights extremists.

Check out the article on page 10 of the December 2005 American Rifleman.

A couple of quotes:

"PETA wants to stop medical advancements that use animal research in any way."

"PETA's agenda is being forced upon society with acts of violence and terrorism . . . This eco-terrorism movement is so dangerous, the FBI has declared it America's No. 1 domestic terrorist threat on American soil . . . Scientists, doctors and their families are having property destroyed and are getting hate mail, letters loaded with razor blades and rat poison, and death threats and bomb threats."

Separate local efforts to kill some of our overpopulated deer herd have met with expensive legal challenges from these people. Hunters at a nearby farm endured multiple instances of vandalism, harassment, and intimidation for each of the last 5 years. I was personally threated in an anonymous phone call. Some of the contributors to our research effort have understandably chosen to remain anonymous even after publication, and we are keeping a lot of information private prior to publication because we believe that the live animal aspects of our work may well be shut down for a time after certain details are released.

Michael Courtney

 

[Shear_stress]

We've also seen major hemorrhaging in unborn fetuses of does shot broadside through the center of the chest

I'm sorry but your research group is somehow able to obtain unborn fetuses on which to perform gunshot-wound experiments?!

Again, your research group should have a list of recent publications that you can reference. What is the name of your research group? Where is it located? Also, please post a link to its website. A Google search turns up nothing.

Science is about disclosure!

Edited to add: The only reference to a "Ballistic Testing Group" I can find on the internet is a link to another one of your posts on the highroad.org!
Edited to add: There is a lot of controverisal research going on at institutes around the country. But they still publish!
Edited once again: If your research is so risky, than why post on a public forum under what we are led to believe is your own name?

 

[Michael Courtney]

I'm sorry but your research group is somehow able to obtain unborn fetuses on which to perform gunshot-wound experiments?!

We shot female deer in a normal (but carefully controlled)hunting-type of situation at a time of year when some test subjects happened to be pregnant. The discovery of severe hemorrhaging of the unborn fetuses was unintentional and accidental, yet we believe that our interpretation of this wounding as a consequence of the pressure wave is valid.

Science is about disclosure!

Science is about disclosing results and sufficient information for other research groups to repeat those results.

It is very common in live animal research projects not to disclose the location, the identity of some contributors, funding sources, photographs, and other details that might provide a target for or attract undue attention from the animal rights fanatics.

Michael Courtney

 

[JohnKSa]

Michael,

Please continue to post your results and please don't be discouraged by the argumentative and confrontational responses of some. Unfortunately, many people aren't interested in discovering the truth unless it aligns with their pre-conceived beliefs and notions.

I think I can say with some level of confidence that there are a large number of people reading this thread with great interest.

Thanks,

John

 

[P95Carry]

there are a large number of people reading this thread with great interest.

That's a fact John Thx again Michael.

 

[RecoilRob]

I don't believe that anyone ever said that a tempory cavity or pressure wave cannot damage tissue. What has been (IMO) proven is that only permanent crushing of important tissue can be reliably counted on to incapacitate a human.

Sometimes the temporary cavity produced by lightweight, fast projos will cause an instant shutdown of the attacker......but manytimes it has not. Repeatedly.

A properly placed, deep penetrating bullet of modest velocity will end all arguments in a fight. Everytime.

And, for the sake of argument, sonic shockwaves can and have done major tissue damage to persons around very loud jet and rocket engines. That is why no-one is allowed near the Shuttle when it launches. They would be injured or killed by the sound alone.

 

[Michael Courtney]

What has been (IMO) proven is that only permanent crushing of important tissue can be reliably counted on to incapacitate a human.

Sometimes the temporary cavity produced by lightweight, fast projos will cause an instant shutdown of the attacker......but manytimes it has not. Repeatedly.

A properly placed, deep penetrating bullet of modest velocity will end all arguments in a fight. Everytime.

Good point. But not even "permanent crushing of important tissue can be reliably counted on to incapacitate a human" within the time span of most gun fights. In other words, incapacitation in the 2-5 second time frame of most gun fights is inherently a probabilistic proposition. Whether or not incapacitation eventually occurs is less important than the likelihood of incapacitation within the duration of the gun fight.

Therefore, a more realistic view of what a bullet should do is to provide the highest probability of incapacitation in a very short time frame. This is why I believe the pressure wave is important: it increases the probabality of incapacitation within the time frame of a gun fight.

In my opinion, increasing the probability of incapacitation in the first five seconds is worth the possible decrease in probability of eventual incapacitation.

For example, (for a given shot placement) a bullet which offers a 50% chance of incapacitaion in 5 seconds or less, but only a 70% chance of eventual incapacitation is a better choice than a bullet which offers a 20% chance of incapacitation in 5 seconds or less but has a 99% chance of eventual incapacitation.

Michael Courtney

 

[RecoilRob]

Somewhere in this or the other related thread Mr. Courtney acknowledges the importance of a deep PCC and this is good. Otherwise, the whole notion of the 'pressure wave' reminds me of the failed RII of the 70's where the TC was held to be the primary incapacitating mechanism and penetration was sacrificed for more TC.

So long as we have deep penetration with corresponding PCC, it does no harm to try to increase the TC. Good luck in your efforts.

 

[Michael Courtney]

Somewhere in this or the other related thread Mr. Courtney acknowledges the importance of a deep PCC and this is good. Otherwise, the whole notion of the 'pressure wave' reminds me of the failed RII of the 70's where the TC was held to be the primary incapacitating mechanism and penetration was sacrificed for more TC.

So long as we have deep penetration with corresponding PCC, it does no harm to try to increase the TC. Good luck in your efforts.

Thanks.

One goal of our work is to try and quantify the relative merits of the PCC and the pressure wave magnitude in order to help people making ammo choices identify the tradeoffs between the two for their own application and risk assessments. Penetration beyond that needed for an application or risk assessment reduces the pressure wave and the temporary cavity and their potential benefits. To little penetration and neither the PCC, the TC, nor the pressure wave has much effect where needed.

An important result of our work is the recognition that if two different loads create comparable permanent crush cavities and penetration depths, the load with more energy and/or more fragmentation is a better bet to create more rapid incapacitation.

An aspect we haven't talked about much is that the PCC and the pressure wave appear to be largely independent incapacitation mechanisms. In other words, the probability of incapacitating via the PCC and the probability of incapacitating via the pressure wave combine by the rules of probability for independent causal factors. For example, if a load has a 50% chance of causing incapacitation via the PCC in under 5 seconds and a 50% chance of causing incapacitation via the pressure wave in under 5 seconds, the combined probability for incapacitation is 75%.

This seems rather academic until one considers the implications for enhancing the incapacitation probability by independent causal effects. In other words, suppose we are able to add an electrical and/or a drug-related incapacitation mechanism to a bullet with a 75% combined probability of incapacitation via PCC and pressure wave. If the drug-related incapacitation mechanism only works 50% of the time, the total incapacitation probability becomes 87.5%. Now add an electrical incapacitation mechanism. If the electrical incapacitation mechanism only works 50% of the time the total incapacitation probability becomes 93.75%.

Now, the idea of drug-related or electrical incapacitation mechanisms might seem far fetched (and they are!), but they serve to illustrate the point that combining a number of unreliable (50%) incapacitation mechanisms can indeed result in much more reliable incapacitation (93.75%) than commonly observed.

Rather than squeezing more reliable rapid incapacitation from the PCC, the improving the status quo lies in increasing and introducing independent incapacitation mechanisms in future bullet designs.

Michael Courtney