Formulating the Pressure Wave Hypothesis

[Michael Courtney]

Earlier posts described the physics of the ballistic pressure wave and provided a definition of stopping power that can be used to investigate possible pressure wave contributions to incapacitation.

It is generally agreed upon that bullet design plays at least as important a role in bullet effectiveness as the cartridge from which it is fired. However, it is still widely debated whether the only contributing factors to the effectiveness of different designs are the volume of crushed tissue and penetration depth. Crushed tissue volume and penetration clearly contribute to bullet effectiveness through the physiological consequences of blood loss. Over the years, a variety of other mechanisms such as hydrostatic shock, energy dump, hydraulic reaction, and the temporary stretch cavity have been suggested. Authors who suggest these mechanisms usually have something in mind more or less related to a ballistic pressure wave. However, these suggested mechanisms have eluded both clear definitions and unambiguous evidence.

The view that the crushed tissue volume (the permanent cavity) is the only reliable contributor to incapacitation (for handgun bullet placements which do not hit the central nervous system or supporting bone structure) relies strongly on the unproven presupposition that easily detectable wounding (see footnote 1) is necessary for an effect to contribute to incapacitation.

Even though it has been shown that most handgun bullets do not produce a temporary stretch cavity (the volume of tissue temporarily pushed out of the way by a passing bullet) large enough to stretch most vital tissue beyond the elastic limit, it remains an unproven presupposition that exceeding the elastic limit is necessary for correlating increased incapacitation with parameters determined from ballistic gelatin.


footnote 1
By this we mean wounding that would typically be detected by a trauma surgeon or medical examiner.


Handgun bullet effectiveness should be studied without depending on the unproven presupposition that the only significant contributors to incapacitation result in wounding that is easily observable to the trauma surgeon or medical examiner. One way to do this is to separate the issue of incapacitation from wounding by directly considering incapacitation and attempting to correlate observed metrics of incapacitation with potential causal agents. Previous work considering wounding or wound trauma as a valid incapacitation metric depends strongly on the unproven presupposition that only easily detectable wounding contributes to rapid incapacitation.

When considering the handgun loads that produce relatively large pressure waves, there is no published data showing that observed measures of rapid incapacitation are correlated only with the volume of crushed tissue or observed wounding. The conclusion that incapacitation is only caused by volume of crushed tissue or observed wounding is not founded upon repeatable experiments or carefully compiled data, but relies only on expert opinion (see footnote 2) and efforts to discredit data suggesting other causal agents.


footnote 2
We agree with Fackler, MacPherson, Roberts, Dodson, etc. on many points, especially their correlations of bullet parameters and gelatin measurements with observed wounding. MacPherson's book is nearly flawless for the ranges of bullet parameters considered. Our scientific disagreement with their work is whether wounding alone is well correlated with rapid incapacitation. To the extent that they don't claim that it is, we are not saying that they are wrong as much as their work is incomplete. (Their claim is that wounding is well correlated with reliable eventual incapacitation. Our concern is rapid incapacitation.) In areas where Fackler, MacPherson, Roberts, Dodson, etc. make assertions based on published data, we agree with almost every assertion they have made. We disagree only with an untested hypothesis for which they offer no data. Such is science. Disagreeing with expert opinion that is not backed up with published data is how scientific progress is made. We kept asking, "Where's the published data correlating rapid incapacitation only to observable wounding?" There isn’t any.



One step in the formation of the pressure wave hypothesis is the fact that most wound ballistics experts agree that a strongly energy-dependent factor such as the temporary stretch cavity plays a vital role in incapacitation via rifle bullets. It is not obvious that this energy dependent disappears as the energy-dependent parameter is lowered from rifle levels to handgun levels. The most powerful service caliber loads only have 20-30% less impact energy than the .223 Remington. (see footnote 3) In addition, some service caliber handgun loads have peak pressure wave magnitudes that are larger than some of the more deeply penetrating rifle bullets.

A second step in the formation of the pressure wave hypothesis is our repeated observations from sport hunting that one only needs a handgun bullet which expands to 0.6” or 0.7” to incapacitate a deer as quickly (with a shot to the center of the chest) as a archery broadhead of 1-3/8” to 1-1/2” cutting diameter. If the only important parameter was the amount of major blood vessels severed to create gradual blood loss, then it stands to reason that a bullet would have to expand to a diameter comparable to that of the broadhead to have a comparable effect.


footnote 3
The most energetic 10mm loads provide over 750 ft-lbs of energy. In an M4, the SS109 round provides 1026 ft-lbs at 50 yards and only 686 ft-lbs at 200 yards. Consequently, studying how incapacitation depends on pressure wave magnitude (related to energy) is also relevant for understanding decreasing .223 effectiveness as range is increased or barrel length is shortened.


Yet with full broadside penetration near the center of the chest, hunting handgun bullets that reliably expand to only 0.6” or 0.7” in the typical deer hunting cartridges will reliably incapacitate deer at least as quickly (on average) as a hunting broad head of 1-3/8” to 1-1/2” cutting diameter. If handgun bullets produce an effect in deer that provides for more rapid incapacitation than bleeding effects alone, it stands to reason that this effect may be present in similarly-sized mammals such as humans.

A third step in the formation of the pressure wave hypothesis is the idea that blood pressure drop due to internal bleeding takes about 5 seconds to have its effect in a best case scenario. Newgard describes this idea well (Ref i):

For an average 70 kg (155 lb.) male the cardiac output will be 5.5 liters (~1.4 gallons) per minute. His blood volume will be 60 ml per kg (0.92 fl. oz. per lb.) or 4200 ml (~1.1 gallons). Assuming his cardiac output can double under stress (as his heart beats faster and with greater force), his aortic blood flow can reach 11 liters (~2.8 gallons) per minute. If one assumes a wound that totally severs the thoracic aorta, then it would take 4.6 seconds to lose 20% of his blood volume from one point of injury. This is the minimum time in which a person could lose 20% of his blood volume.

We agree with this assertion, and the theoretical ideas are confirmed by many observations of deer almost always taking 5-10 seconds to fall with any broadside archery shot hit through the center of the chest. In contrast, we have observed numerous deer drop in under 5 seconds when hit by handgun bullets creating pressure waves at the larger end of the spectrum. Likewise, events of apparently involuntary incapacitation in under 5 seconds are repeatedly reported in humans for handgun shots which fail to hit the CNS or supporting bone structure.

The Strasbourg Tests (Ref ii) employed a pressure sensor inserted into the carotid artery of live unanaesthetized goats. These tests directly suggest that an internal pressure wave created by the interaction of the bullet and tissue can contribute to rapid incapacitation and can incapacitate more quickly than the crush cavity/blood loss mechanism alone:

In a substantial number of cases, the subject was incapacitated almost instantly. Each time this occurred, between two and five pressure spike tracings of high amplitude and short duration were found which immediately preceded and matched corresponding, diffused, or flattened lines (EEG tracings). Normally, the time lag between the first pressure spike and the beginning of slowed or flattened lines was between 30 and 40 milliseconds (although there were several cases where this delay lasted as long as 80 milliseconds)…The taller pressure spike tracings always preceded the slowed or flat line tracing…The initial spikes had to be of a certain height in order for the animal to collapse immediately.

However, the anonymity of the experimenters and has resulted in ongoing doubt about the findings.

In contrast to the Strasbourg result, there have been some arguments against the pressure wave hypothesis. Claims to disprove the hypothesis of pressure wave incapacitation effects usually contain one or more of the following flaws:

1. Considering velocity ranges rather than pressure wave magnitude ranges. There is no velocity threshold where the pressure wave effects begin to turn on. There is a pressure wave magnitude threshold.

2. Considering observable wounding rather than a measure of incapacitation. It is important to consider the possibility of incapacitation mechanisms that might not produce wounding that is easily detectable to a trauma surgeon or medical examiner. Consequently, to disprove the pressure wave hypothesis, one would have to observe and measure incapacitation directly rather than simply observing wounding after the fact. To our knowledge, there is no published data that fails to show a pressure wave contribution to incapacitation over the full range of peak pressure magnitudes produced by handgun loads.

3. Showing that the pressure wave does not make a significant contribution to incapacitation in a pressure wave regime considerably smaller than some available handgun loads. To compare different handgun loads, we consider the peak pressure on the edge of a 1" diameter circle centered on the axis of the wound channel. Handgun loads that produce 500 PSI at this point have pressure wave incapacitation effects that are difficult to discern (require a very large number of data points) with shots to the thoracic cavity. Handgun loads that produce over 1000 PSI at this point and penetrate at least 10" have pressure wave contributions that are relatively easy to discern (don't require as many data points.)

4. Confusing the concepts of unproven and disproven. The fact that some previous studies make a weak case for the pressure wave mechanism, means that the effect has not yet been proven in the published literature. This does not mean it has been disproven.

5. Considering kinetic energy ranges rather than pressure wave ranges. It is not sufficient to show the absence of a pressure wave contribution to incapacitation with loads that produce a certain amount of kinetic energy. Disproving the pressure wave hypothesis requires showing the absence of a pressure wave contribution to incapacitation with loads that produce 1500 PSI on the edge of a 1" diameter circle centered at the wound channel.

6. Considering only the "sonic pressure wave" rather than the complete pressure wave (defined as the force per unit area that would be measured by a high-speed pressure transducer).

Consequently, since there has been no convincing experimental disproof of the pressure wave hypothesis, we should consider that the hypothesis of a pressure wave contribution to rapid incapacitation has substantial anecdotal support, and is well supported by an anonymous experiment of questioned veracity (the Strasbourg Tests).

There are also a number of papers in the peer-reviewed journals discussing ballistic pressure wave effects on wounding and incapacitation (Ref iii). These papers are mainly concerned with velocities of rifle bullets, but the energy and pressures produced are within the regime of pistol bullets.

Suneson et al. report that peripheral high-energy missile hits cause pressure changes and damage to the nervous system. This experimental study on pigs found that test subjects shot in the left thigh (516 ft-lbs of energy transferred) experienced pressure waves in the brain on the order of 18 PSI. Apneic periods were observed during the first few seconds after the shot, and both blood-brain and blood-nerve barrier damage were found. They concluded that “distant effects, likely to be caused by the oscillating high-frequency pressure waves, appear in the central nervous system after a high-energy missile extremity impact.”

Martin Fackler published a reply in both the Journal of Trauma and Wound Ballistics Review (Ref iv), asserting that “Shock Wave” is a myth:

In ascribing “local, regional, and distant injuries” to the sonic pressure wave, Suneson et al. have overlooked the effect of transmitted tissue movement from temporary cavitation. Since two distinct mechanisms are acting in the Suneson et. al experiment, one cannot arbitrarily assign any effects observed to only one of them.

Fackler’s replies have several major flaws:

• Fackler employs the straw man fallacy by referring to the pressure wave studied by Suneson et al. as “the sonic pressure wave.” The authors studied a “shock” wave and clearly stated that the wave includes both sub-sonic and super-sonic frequency components up to 250 kHz. By definition, sonic waves only include frequencies from 20 Hz - 20 kHz. The pressure wave under study has both sonic and super-sonic components. In addition, Fackler considers the “sonic pressure wave” to be limited to a very short (several microseconds) pulse that preceeds temporary cavitation. Suneson et al. are describing effects of pressure waves with a much longer duration.
  
• Fackler creates a false dichotomy to divide effects beyond the permanent crush cavity into only the temporary cavity and the “sonic” pressure wave. Ballistic pressure waves have components both at frequencies below the sonic range (< 20 Hz), and at frequencies above the sonic range (> 20 kHz). The pressure wave consists of every force per unit area that can be detected by a high-speed pressure sensor.
  
• Movement of tissue by cavitation is not distinct from the ballistic pressure wave. (One can consider temporary cavitation an effect of the inertial component of the pressure wave.) Consequently, ascribing the local neural injuries to the pressure wave is not unreasonable, though Fackler is correct to point out that in the local region, the pressure wave effects cannot be distinguished from temporary cavitation effects.
  
• Suneson et al. also report regional and distant effects beyond the reach of the temporary cavity. Nerve damage is observed as far as 0.5m away from the wound channel. These regional and distant effects cannot be ascribed to temporary cavitation.

Fackler continues:

Recently, eleven adult human-sized swine (90 kg) were shot in the proximal part of the hind leg with a projectile producing the damage profile of the Russian AK-74 Assault rifle bullet. This same projectile was used in another study in which five 90 kg swine were shot through the abdomen …No indication of any sort of “distant” damage was seen in the pigs’ behavior and no “distant” injuries were found at autopsy.

The methodology of Fackler’s pig experiments is significantly different from Suneson et al., who report that the neural damage is not easily observable, but rather depends upon examination with light and electron microscopy. The effects that Suneson et al. report “were evident a few minutes after the trauma and persisted even 48 hr after the extremity injury.” In Fackler’s experiments, autopsies were not performed until weeks or months later. With such great differences in experimental methodology, it is unfounded to assert that Fackler’s swine experiments contradict the conclusions of Suneson et al.

Fackler continues:

A review of 1400 rifle wounds from Vietnam (wound Data and Munitions Effectiveness Team) should lay to rest the myth of “distant” injuries. In that study, there were no cases of bones being broken, or major vessels torn, that were not hit by the penetrating bullet.

It strains that boundaries of credulity that someone would refute modern observations (using new methods) of microscopic damage to nerve cells by referring to the absence of observations of broken bones or torn blood vessels in a Vietnam-era observations from trauma surgeons. The Vietnam-era study was not looking for distant nerve damage, and they did not employ the methods used by Suneson et al.

The results of Suneson et al. also find substantial agreement with later experiments in dogs conducted by an independent research group using a substantially similar methodology (Ref v).

There are a number of additional papers in the peer-reviewed journals studying the damage to the central nervous system caused by pressure wave effects. Since their focus is on long-term effects, this research does not reach definitive conclusions regarding whether these pressure wave effects contribute to rapid incapacitation of humans. However, there is a growing body of evidence that pressure waves near 30 PSI can cause CNS damage that would usually be undetected by a trauma surgeon or medical examiner, but can be quantified with advanced neurological techniques.

There is also well-established evidence that pressure waves near 30 PSI applied to the brain causes immediate incapacitation of laboratory animals (Ref vi). In a study applying a pressure wave directly to the brain via the lateral fluid percussion technique, Toth et al. report both instantaneous incapacitation and cellular damage:

The delivery of the pressure pulse was associated with brief (<120-200 sec), transient traumatic unconsciousness (as assessed by the duration of suppression of the righting reflex).

One reasonably wonders what relevance these live animal experiments using the lateral fluid percussion technique to induce a pressure wave injury in laboratory animals have for understanding neurological pressure wave effects in humans. A 15 year review and evaluation of this question concluded (Ref vii):


We conclude that the lateral fluid percussion brain injury model is an appropriate tool to study the cellular and mechanistic aspects of human traumatic brain injury…

Consequently, there is significant support for the hypothesis of a pressure wave contribution to incapacitation not only in anecdotal observations and an anonymous experiment on goats, but also in well-established results of neurological experiments.

As of January 2006, there are published results showing that a pressure wave can cause rapid neurological incapacitation and/or damage in goats, dogs (Ref viii), swine, several species of laboratory rats, and even in whales (Ref ix). In many of these cases, detecting wounding requires advanced techniques such as electron microscopy, cellular analysis, EEG monitoring, and sophisticated chemical analysis. Consequently, the hypothesis that incapacitation only occurs from wounding that is easily detectable to the trauma surgeon or medical examiner has been disproven. This opens the door to consider support for pressure wave contributions to incapacitation by experiments observing incapacitation directly without concern for easily detectable wounding.

Michael Courtney

 

[Michael Courtney]

References for previous post

REFERENCES:

i Newgard, Ken, M.D.: "The Physiological Effects of Handgun Bullets: The Mechanisms of Wounding and Incapacitation." Wound Ballistics Review, 1(3): 12-17; 1992.

ii The Strasbourg Tests, Anonymous report of the Strasbourg Goat Tests, first openly presented at the 1993 ASLET International Training Conference, Reno, Nevada.

iii Göransson AM, Ingvar DH, Kutyna F: "Remote Cerebral Effects on EEG in High-Energy Missile Trauma". The Journal of Trauma. 28(1 Supplement):S204-S205; January 1988.

Suneson A, Hansson HA, Kjellström BT, Lycke E, and Seeman T: "Pressure Waves by High Energy Missile Impair Respiration of Cultured Dorsal Root Ganglion Cells". The Journal of Trauma. 30(4):484-488; 1990.

Suneson A, Hansson HA, Seeman T: "Pressure Wave Injuries to the Nervous System Caused by High Energy Missile Extremity Impact: Part II. Distant Effects on the Central Nervous System. A Light and Electron Microscopic Study on Pigs". The Journal of Trauma. 30(3):295-306; 1990.

Suneson A, Hansson HA, Seeman T: "Pressure Wave Injuries to the Nervous System Caused by High Energy Missile Extremity Impact: Part I. Local and Distant Effects on the Peripheral Nervous System. A Light and Electron Microscopic Study on Pigs". The Journal of Trauma. 30(3):281-294; 1990.

Suneson A, Hansson HA, Lycke E: "Pressure Wave Injuries to Rat Dorsal Cell Ganglion Root Cells in Culture Caused by High Energy Missiles". The Journal of Trauma. 29(1):10-18; 1989.

Suneson A, Hansson HA, Seeman T: "Central and Peripheral Nervous Damage Following High-Energy Missile Wounds in the Thigh". The Journal of Trauma. 28(1 Supplement):S197-S203; January 1988.

Suneson A, Hansson HA, Seeman T: "Peripheral High-Energy Missile Hits Cause Pressure Changes and Damage to the Nervous System: Experimental Studies on Pigs". The Journal of Trauma. 27(7):782-789; 1987.

iv Fackler ML, “Letter to the Editor”, Journal of Trauma, 29(10):1455, 1989.

Fackler ML, “Literature Review and Comment”, Wound Ballistics Review, Winter 1991: pp38-40.

v Wang Q,Wang Z, Zhu P, Jiang J: “Alterations of the Myelin Basic Protein and Ultrastructure in the Limbic System and the Early Stage of Trauma-Related Stress Disorder in Dogs. " The Journal of Trauma. 56(3):604-610; 2004.

vi Toth Z, Hollrigel G, Gorcs T, and Soltesz I: “Instantaneous Perturbation of Dentate Interneuronal Networks by a Pressure Wave Transient Delivered to the Neocortex.” The Journal of Neuroscience, 17(7);8106-8117; 1997.

vii Thompson HJ, Lif????z J, Marklund N, Grady MS, Graham DI, Hovda DA, McIntosh TK, “Lateral Fluid Percussion Brain Injury: A 15-Year Review and Evaluation”, Journal of Neurotrauma, 22(1):42-75 (2005).

viii Wang Q,Wang Z, Zhu P, Jiang J: “Alterations of the Myelin Basic Protein and Ultrastructure in the Limbic System and the Early Stage of Trauma-Related Stress Disorder in Dogs. " The Journal of Trauma. 56(3):604-610; 2004.

ix Knudsen SK, Oen EO: “Blast-induced neurotrauma in whales.” Neurosci Res. 46(3): 377-386 (2003).

 

[lbmii]

Velocity is a major component in terminal ballistics. The big question is to what extent is velocity a factor in handgun bullet terminal ballistics?

I suspect velocity plays a bigger role in handgun terminal ballistics than what many think.

I suspect that blunt bullets accelerate tissue in a radiating cone in front of and to a smaller extent to the sides of the bullet. I suspect that a permanent crush cavity is created where the acceleration forces on the tissue exceeds the shear strength of the tissue and in some cases the tensional strength of the tissue. The line where the permanent crush tissue ends is where the acceleration forces and the shear strength of the tissue are in equilibrium.

The more volume of tissue a bullet can impart velocity onto (wide blunt bullet), and the more velocity the tissue can be accelerated to (fast bullet) the larger the permanent crush cavity you will get. Some tissue by its' nature will be more susceptible to the forces caused by acceleration imparted onto it by a bullet.

Then one also must take into consideration the shock waves that radiate out from the bullet and spreads throughout the various tissues. Many dismiss these shock waves as being too minor when it comes to handgun bullet terminal ballistics. I suspect the shock waves can play a role in certain cases where the shockwaves do not readily dissipate such as inside the cranium or to a lesser extent inside the upper chest cavity. Many of us here have seen grisly photos of massive head trauma (popped like a balloon) caused by 357 Magnum rounds. But a 357 Magnum round that transverses a similar depth of tissue say in an upper thigh will produce a much smaller wound.

Some volume of controversy arises when one postulates that the shock waves that radiate out from a bullet can disrupt the nervous system to a significant degree even when the bullet strikes an area away from major nerve locations. I am personally a bit doubtful, especially when concerning handgun bullet terminal ballistics.

 

[MCgunner]

Whew, my God, I haven't felt this much brain drain since my comparative chordate anatomy class.

I have suspected all along that velocity has more to do with incapacitation than the big/slow bullet guys wanna admit, especially as velocity exceeds 1000 ft/sec. My deer hunting experiences with rifles and hand guns have also taught me to suspect the big bullet momentumists. I've hunted with and killed deer with the .357 magnum. It's making only about 700 ft lbs, but moving around 1400 fps in my loads. While I've not killed deer with a .44 special or .45acp standard loads out of respect for the game, I have noted the tissue trauma from the pistols and various rifle calibers I've used.

What is amazing is the 7mm magnum, which I've seen with chest cavity hits totally destroy any remnant of lungs in the chest. I just gotta figure since that little bullet didn't hit ALL the lung, there had to be a pressure wave or something that was the cause for this tissue destruction. While the big bullet types discount rifle terminal ballistics as irrelevant, I don't understand how it's irrelevant. It shows that more energy/velocity means more pressure wave damage, to me. Even out of SWC flat nosed .357 bullets, I'll get total lung tissue destruction 3" in radius away from the actual wound channel. I've SEEN it! Okay, I'm no forensic expert, but how can you ignore what you see with your own eyes? There has to be energy transfer causing this by one mechanism or another. A bullet needs energy to cause damage. Kinetic energy and the amount of it that is delivered has always seemed most important to me, not bullet momentum.

All the momentum formulas made up out of thin air by guys like Chuck Taylor smack of a big bullet agenda, to me. Momentum transfer is important for knocking pins off tables or knocking over pepper poppers, but energy and energy transfer is what looks like it's destroying the tissue in all the deer I've ever lung shot.

This was a good treatise on the subject. Like I say, I'm no expert, just gotta believe my eyes when I shoot something. I really don't care anymore what does the actual killing, because I know what works on game animals and if it works on game animals it should work on humans. I'll hunt deer anytime with the .357 magnum, but won't use lesser SD calibers. To me, nothing beats the .357 for fight stopping effectiveness. If I can't use the .357 or 10mm in an effectively concealable firearm, I'll pick something that comes as close as possible. The 9mm +P I fire out of my small 9mm approaches 400 ft lbs and 1200 fps with a 115 grain hollow point. It should do a little more tissue damage than a .38 and at LEAST as much as the best .45s and I ain't no hardball shooter. I don't use hardball on deer and I danged sure ain't gonna use it on an attacking human. I wanna kill the guy, not irritate him. I've had rifle caliber bullets fail to expand and have to blood trail a deer for hundreds of yards before. That experience tells me something about bullet performance and energy transfer, too.

 

[pest3125]

In Michael's text - it is unclear to me if the "center of mass shots" that miss the central nervous system are assumed to hit the heart or not.

If the center of mass shots are assumed to hit the heart, then I don't know what the big deal is - it seems to me that a shot that penetrates deeply enough to hit the heart (or cuts the aorta) will lead to incapacitation in 5 seconds or so due to blood pressure loss (as Michael indicates). Since the heart is filled with blood, which is basically incompressible, a projectile with enough energy may burst the organ (like shooting a water filled milk jug). Nothing special here - even a 9mm HP can burst a water filled jug.

If the center of mass shots are assumed to miss the heart (or its major entrance/exit blood vessels) *and* miss the spine - I am wondering what Michael's theory is - will the "pressure wave" still result in physiological incapacitation in 5 seconds? I suppose its possible, the shock to the heart from a projectile passing nearby can cause the heart to stop or have irregular rhythms, still I don't see if there is anything so new or novel about that.

 

[MCgunner]

The Facklerites argue that nothing matters other than the actual tissue the bullet touches, that there's no other tissue damage. If you hunt and clean your own game, after a while, you'll realize the BS in that assumption. There is tissue damage AWAY from a bullet. The amount seems to relate to energy transfer. Call it "pressure wave" or "hydraulic shock" or whatever, there is a mechanism at work here related to energy transfer, IMHO.

But, unless you nit pick over such things for the pure academic fun of it or you're trying to support the statement that slow and big is better than smaller and faster (and more energetic 'cause energy is a function of the square of the velocity), just shoot for center mass with something that measures 9mm in diameter or better and don't worry about it. Just pull the trigger until the attack stops.

 

[Feanaro]

The Facklerites argue that nothing matters other than the actual tissue the bullet touches, that there's no other tissue damage.

I've never seen any such thing stated by Fackler. While discussing the M193 woud pattern in "Patterns of Military Rifle Bullets", he notes that "The temporary cavity stretch, its effect increased by perforation and weakening of the tissue by fragments, then causes a much enlarged permanent cavity by detaching tissue pieces." He even speculates on whether a three round burst fired at 2000 rpm(as in the H&K G11) could cause the temporary cavities to have a synergistic effect.

"Facklerites" may not be on the same page, of course. Though I've heard pleny of hokum-bokum from hydrostatic shock(or whatever you want to call it) believers.

Anyways, I will be following this with interest. I'd like to see the results, one way or the other.

 

[Michael Courtney]

In Michael's text - it is unclear to me if the "center of mass shots" that miss the central nervous system are assumed to hit the heart or not.

The pressure wave radiates outward in all directions and impacts many organs and tissues not directly hit by the bullet. Some of the references above find significant injury to the central nervous system due to pressure waves, and the pressure wave hypothesis is based on the strength of the evidence that the a pressure wave can disrupt the CNS without the bullet hitting it directly.

If the center of mass shots are assumed to miss the heart (or its major entrance/exit blood vessels) *and* miss the spine - I am wondering what Michael's theory is - will the "pressure wave" still result in physiological incapacitation in 5 seconds?

The probability of a pressure wave causing incapacitation in under 5 seconds increases with the magnitude of the pressure wave. Bullets which produce larger pressure waves have a higher likelihood of creating this kind of incapacitation than bullets with smaller pressure waves.

I suppose its possible, the shock to the heart from a projectile passing nearby can cause the heart to stop or have irregular rhythms, still I don't see if there is anything so new or novel about that.

Stopping the heart or inducing irregular rhythms is unlikely to be effective in under 5 seconds. Creating incapacitation in under 5 seconds more likely requires an interruption of the nervous system.

Michael Courtney

 

[porterdog]

That was dense but remarkably readable- well done!

 

[ShelbyV8]

There is a difference in stopping power and deadly shots. A shock wave near the heart and artires that can cause a spike in blood pressure which can cause disorentation or unconciousness. A jab to the chest or judo chop which has no penetration does just this. Just stopping the heart leaves about 30 seconds of fight in person, in this amount of time I can fire 46 rounds out of a hicap 9mm or empty a shotgun.

 

[james481]

The 9mm +P I fire out of my small 9mm approaches 400 ft lbs and 1200 fps with a 115 grain hollow point. It should do a little more tissue damage than a .38 and at LEAST as much as the best .45s and I ain't no hardball shooter.

Good post, I only disagree with this part. I'm not sure what .45 loads you are referring to, but your statement seems in error. Out of my Glock 30, a DT 185gr GDHP makes 1160 fps for about 600 ft/lbs. So even if you believe that velocity heavily affects wounding potential, this load is only 40 fps slower, and the extra .2 inches (expanded) and 200 ft/lbs of energy certainly couldn't hurt.

 

[thales]

*


Dr. Courtney, I applaud your patience.

About 35 years ago I shot a deer with a Remington 180gr pointed softpoint in 30-06 at a range of approximately 50 yards. The deer, a Pacific blacktail of about 100 pounds live weight dropped instantly in its tracks and didn't twitch. It took me roughly one to two minutes to get to the deer, which was dead at that point. The bullet entered the left thorax of the deer about one or two inches above the horizontal midline of the thorax, about midway between the heart and the diaphragm. The bullet angled slightly downward and exited the right side. It was not recovered. The posterior portion of both lungs was severely disrupted, but I saw no visible damage to the heart, spine, vena cava, portal vessels, or abdominal aorta. There was, of course, a good deal of blood in the pleural cavities, roughly one quart, as I recall. I don't know if that amount of blood loss was sufficient to kill the deer. Keep in mind that this was quite some time ago, before I took an anatomy class, and I wasn't observing in detail and taking notes.

The reason that I am sharing this anecdote is that the existing models of gunshot wound incapacitation that I have seen are inadequate to explain it. Having seen this phenomenon, which I estimate as reasonably common among experienced hunters, I am less skeptical than others might be about similar reports. I do not automatically dismiss the Strasbourg study as a fraud, for example.

In the intervening years, I have considered a number of hypothetical mechanisms to explain instant gunshot incapacitation in cases like this. They include a pressure wave damaging the brain via the spinal cord or circulatory system, a pressure wave damaging the heart and major arteries directly, a temporary stretch cavity causing stretching of the heart directly causing cardiac arrhythmia or fibrillation, stretching of the heart, blood vessels or the diaphragm causing a generalized nociceptive inhibition reflex, and stretching of internal organs causing neurovascular shock mediated by the autonomic nervous system, etc.

One major complaint that I have regarding popular incapacitation models, is that they show very little consideration for physiological mechanisms, and what they do show is often oversimplified or inaccurate. Dr. Fackler, for example, repeatedly refers to "heart tissue". The heart is an organ which contains several tissues, including cardiac muscle tissue, smooth muscle, endothelium, connective tissue, nerve fibers, etc. The distinction is highly relevant to incapacitation mechanisms because the tensile strength and reaction to pressure or stretch of different tissues, important ones, within an organ may vary considerably. Nerve fibers are likely to have considerably lower tensile strength than do muscle fibers and connective tissue. So a muscle that shows no obvious damage in gross may include irreversibly damaged nerve fibers. Nerve fibers may be strongly stimulated at considerably lower stretch or pressure levels than would damage them, even temporarily. I suppose it is constructive at this point to mention as an aside that there are medical conditions wherein affected people may faint after eating or urinating. The stimulus that causes the fainting is the change in pressure in the relevant organs, mediated by the nervous system.

In view of the foregoing, I would recommend that you include medical scientists or neurophysiologists on your team (maybe you already have done so) in order to help keep your work steered into productive ground.

I enjoy your posts and I look forward to the publication of your book. (There is a book coming, isn't there?) Good luck and please keep posting in spite of the flack.


*

 

[ghost squire]

it remains an unproven presupposition that exceeding the elastic limit is necessary for correlating increased incapacitation with parameters determined from ballistic gelatin.

Could you rephrase that please, I don't understand.

footnote 3
The most energetic 10mm loads provide over 750 ft-lbs of energy. In an M4, the SS109 round provides 1026 ft-lbs at 50 yards and only 686 ft-lbs at 200 yards. Consequently, studying how incapacitation depends on pressure wave magnitude (related to energy) is also relevant for understanding decreasing .223 effectiveness as range is increased or barrel length is shortened.

The .223 is largely dependant on fragmentation to wound/kill. Fragmentation is dependant on the bullet yawing, at which point the forces exerted on it by its velocity through flesh will cause it to fragment, creating a very large permanent wound cavity. So the slower it goes, the less it fragments and therefore wounds, until a point at which it no longer fragments and is the equivalent of a .22 going through someone. My point being that was a poor choice for an analogy.

to incapacitate a deer as quickly (with a shot to the center of the chest) as a archery broadhead of 1-3/8” to 1-1/2” cutting diameter. If the only important parameter was the amount of major blood vessels severed to create gradual blood loss, then it stands to reason that a bullet would have to expand to a diameter comparable to that of the broadhead to have a comparable effect.

Obviously. Which is why its common sense to shoot for the vitals... Such as the heart, more specifically.

Compare the volumes of the two wounds in a relatively homogenous structure such as human muscle tissue (which the heart is largely composed of), or ballistic gelatin. Are they not relatively the same? We're talking about thin but long little blades compared to a cylinder exactly such and such in diameter. They will destroy about the same amount of tissue.

In contrast, we have observed numerous deer drop in under 5 seconds when hit by handgun bullets creating pressure waves at the larger end of the spectrum. Likewise, events of apparently involuntary incapacitation in under 5 seconds are repeatedly reported in humans for handgun shots which fail to hit the CNS or supporting bone structure.

Thousands of people have dropped dead instantly after being shot with a .22. I'll stick by what I said, involuntary collapse, fainting in effect. It doesn't really matter because its unpredictable right now. Don't rely on your handgun to instantly incapacitate someone! Until the effects can be reproduced 100 percent of the time.

I have no doubt that "pressure waves" have something to do with incapacitation and wounding in handguns cartridges. What exactly that is I don't know, and don't plan to rely on it until I've seen it can do it reliably.

Time and time again history has proven that against a determined or drugged up foe, its hard to beat either a rifle or the widest handgun bullet you can get your hands on.

 

[MrAcheson]

With all due respect I find some of your work here very weak. For instance you really don't seem to have an adequate understanding of wave propogation phenomenon.

When you refer to a sonic shock or sonic wave, it is not "sonic" in the sense that it is made up of frequencies found in the human auditory spectrum. It is "sonic" in that it is a compression wave which propogates through a medium at that medium's speed of sound.

There is no such thing as a super-sonic compression wave, the speed of sound is the upper limit. Nor can you create a shock wave in an incompressible medium like the human body. This is why hydrostatic shock is a misnomer even if there may be some truth to the behavior. In fluid mechanical terms, it is neither hydrostatic nor a shock. The phenomenon itself may cause shock (as in the medical term), but that is something different.

There are other problems as well of course, for instance the wound mechanics of a broadhead arrow are almost completely different than those a handgun round. I realize you are trying to compare a projectile that creates a pressure wave (the bullet) to one that does not (the arrow). While that is fine conceptually, any comparison of stopping power for a given wound size (as you do) is bound to be flawed because you lack a control variable. There are more differences between an arrow wound and a bullet wound than just the presence of a pressure wave. Just the inclusion of the arrows shaft and how it alters bleeding changes things tremendously.

There are also problems with your "flaws." For instance many of Fackler's "flaws" are simply attempts to concentrate research on variables which can be adequately measured experimentally, like wound volume, bullet expansion, and penetration. Variables like incapacitation can have large disparaties between individual test subjects and also require relatively expensive in vivo testing.

Your post isn't bad work, but I really think it needs some revision.

 

[thales]

*


I am under the impression that measuring incapacitation is the whole object of these difficult and expensive exercises.


*

 

[MCgunner]

About 35 years ago I shot a deer with a Remington 180gr pointed soft point in 30-06 at a range of approximately 50 yards. The deer, a Pacific blacktail of about 100 pounds live weight dropped instantly in its tracks and didn't twitch. It took me roughly one to two minutes to get to the deer, which was dead at that point. The bullet entered the left thorax of the deer about one or two inches above the horizontal midline of the thorax, about midway between the heart and the diaphragm. The bullet angled slightly downward and exited the right side. It was not recovered. The posterior portion of both lungs was severely disrupted, but I saw no visible damage to the heart, spine, vena cava, portal vessels, or abdominal aorta. There was, of course, a good deal of blood in the pleural cavities, roughly one quart, as I recall. I don't know if that amount of blood loss was sufficient to kill the deer. Keep in mind that this was quite some time ago, before I took an anatomy class, and I wasn't observing in detail and taking notes.

The reason that I am sharing this anecdote is that the existing models of gunshot wound incapacitation that I have seen are inadequate to explain it. Having seen this phenomenon, which I estimate as reasonably common among experienced hunters, I am less skeptical than others might be about similar reports. I do not automatically dismiss the Strasbourg study as a fraud, for example.

I think anyone who has hunted has experienced such things. I know I've lung shot deer, had 'em collapse almost immediately, open 'em up and can't find much left of lung tissue. This was a very rapidly expanding 150 grain bullet in a 7mm Rem Mag. I've shot deer with .357 magnum handgun bullets. I once used my own cast, gas checked SWC on a deer about 80 yards away from my lever carbine. The bullet, by the time it reached the target, was at handgun velocities. It entered behind the shoulder through the lungs and left the off side ribs. Upon examination there was a 3-4 inch channel diameter around the path of the actual bullet where the lung tissue was completely destroyed. I'm thinking pressure wave off that flat point bullet, which no doubt did not expand. It was definitely energy transfer of some process. The deer made it about 25 feet before dropping, seconds until total incapacitation and the bullet never touched anything, but lung tissue. It did break a rib on the way out, but went between ribs on the entrance.

To me, fackler doesn't adequately address such wounding away from the bullet. And, people like Taylor with their momentum based arithmetic are so completely full of it, makes me wanna puke. There is energy transfer going on here. It has nothing to do with bullet momentum. This is just pure logic. I don't need to be a physicist to figure this one out. I'm not schooled in the subjects adequately enough with my BS/biological sciences background to try to sound like some sort of expert, but I have opinions on the subject just like Chuck Taylor who sounds as if he has even less education on the subject when you read his drivel.

I took plenty of statistics in school, statistics being the major way to analyze such as indirect population counts of fishes in a lake, that sort of thing. You have to be able to determine a mean, a variance, or calculate linear regression lines to determine trends, so I was schooled in such. I know statistics is only as good as the data that is being analyzed. However, I've always put more faith in actual gunfight statistics than in gelatin. Given enough data, a trend will form, a mean will be established, and statistical variance can be calculated and analyzed for such data. At least THAT is something I can understand. And, when Marshall says .45 hardball has a 60% one shot stop (whatever the definition of that is) ratio, well, that's something I can sink my teeth into. When he says the best hollow points come in around 90%, that makes complete sense to me in that the bullet is transferring more energy, creating a pressure wave or however it does it, to tissue. IOW, the wounding and tissue damage is greater. Shoot a squirrel with a solid point .22, then shoot one with a hollow point and note the meat damage. I learned even as a 10 year old kid that if I didn't want total destruction of the upper part of the squirrel, not only should I strive for head shots, but I should use solids. I also noted that hollow points stopped rabbits NOW! Solids weren't up to the job. I was a pre-teen, but that lesson sunk in!

Anyone that hunts knows there's more to wounding than just bleeding, a lot more. Like I say, I'll let you experts hack such things out. I've got no education in such. I'm just a mechanic at this point, a mechanic with a BS in Fisheries Management, but a mechanic.

 

[The_Antibubba]

Interesting timing

There's an article in American Scientist this month about advances in the photography of shock waves; there are some megacool pictures of firearms being fired.

 

[MCgunner]

Hmm, wonder if that's online somewhere? Sounds good.

Want to add my OWN reasons for caring about such arguments. To me, it's not the size of the projectile because I think two things are important in a hunting caliber for a given size of game OR a human in a self defense scenario. One is bullet energy and the other is energy transfer on target. This is why the old axiom 1000 ft lbs for deer on target. This is why nobody hunts deer with a full metal jacket bullet (lack of energy transfer). Being a hunter, I carry this over to choices in self defense. Of course, there's more to the choice that caliber or I'd carry a 7mm rem mag wherever I went. The platform has to be concealable. But, in hanguns, TWO, possibly THREE calibers stand out to me, the 10mm, the .40, and the .357 magnum. In defense loads, they are all over 550 ft lbs from service size guns and all have a good range of hollow point bullets to deliver that energy. That's where my trust goes. Between 9mm and .45, they both have about the same energy and the added velocity of the 9 means it will better and more reliably open a hollow point to transfer that energy. Right now, I'm working on getting a carryable 3" .357 magnum, preferably a Ruger SP101. In autos, the .40 might well offer the most power in the smallest package in such guns as the Glock 27, but I think the .40 is a little hard on small guns. However, it's a good caliber. The 10 is strictly a service size gun caliber, but it's mighty powerful with 700 ft lbs on tap. The .357 is capable of as much when hand loaded.

Regards to bullet diameter, I fail to see any reason why it should matter, really. In a flat point bullet of the same profile as a smaller bullet, it will, of course, transfer more energy. However, the .45 is but one tenth of an inch larger than the 9mm/.357 bullet. That's just a little over half the diameter of a BB! Woopty do! Don't take much more bullet expansion to equal that and regardless, the bullet with the most energy needs less energy transfer to put an equal amount of energy on target. If you're pushing a 140 grain bullet at 1400 fps (a handload of mine), you're pushing over 600 ft lbs. With the .45 ACP, you've got under 400 ft lbs to play with. That's over 200 ft lbs difference. This is why the .357 or the 10mm is often used to hunt medium game with and the .45 is not considered adequate for such, not until you push it with a LARGE charge of H2400 in a .45 colt case, anyway.

So, anyway, right now I've been really Jonesin' for a SP101 3" in .357. Maybe sometime this year I'll pick one up. I've dismissed the 2" ones because of excessive muzzle flash and not a lot of umph over a +P .38 out of that short of a tube. Don't know what it is, but add and inch to the barrel, and the .357 is a whole nuther animal. Somewhere in that inch, a lot of that slow burning powder gets burned, apparently. The chronograph don't lie.

 

[Michael Courtney]

With all due respect I find some of your work here very weak. For instance you really don't seem to have an adequate understanding of wave propogation phenomenon.

I have a PhD in Physics from the Massachusetts Institute of Technology and my area of speciality is wave propagation.

The folks I have quoted seem to have an inadaquate understanding of wave propagation phenomena, but I try not to nit pick about word definitions unless it is critical to the evaluation of an article's validity.

One might think that someone suggesting that a Physicist "doesn't seem to have and adaquate understanding of wave propogation phenomenon" would know how to spell the word, "propagation" and also know to use the plural "phenomena" because there are lots of waves which do lots of things.

When you refer to a sonic shock or sonic wave, it is not "sonic" in the sense that it is made up of frequencies found in the human auditory spectrum. It is "sonic" in that it is a compression wave which propogates through a medium at that medium's speed of sound.

Other than quoting others, I do not refer to the ballistic pressure wave as a "shock" wave. I also do not refer to the ballistic pressure wave as a "sonic" wave other than when quoting others. Both terms are imprecise and mean different things depending on the field of study and the background of the person reading.

I refer to a "ballistic pressure wave" which I define for practical purposes to be the force per unit area that can be measured by a high-speed pressure gage.

My point is that the ballistic pressure wave cannot be limited to a "sonic wave" regardless of whether one defines the "sonic wave" as all the pressure wave components that propagate at the speed of sound or as the frequency components within the audio spectrum. Fackler is making a false dichotomy using either definition.

In addition, if Fackler intends "sonic" to mean all frequency components propagating at the speed of sound in the medium, he should say so explicitly. (In the literature "sonic" means "within the audible hearing range" more often than it means "propagating at the speed of sound in the medium.")

But the bottom line is that there is more to the ballistic pressure wave than the "sonic" pressure wave, regardless of which definition of "sonic" is intended.

There is no such thing as a super-sonic compression wave, the speed of sound is the upper limit. Nor can you create a shock wave in an incompressible medium like the human body.

I never said that there is a super-sonic compression wave or that the ballistic pressure wave is a "shock wave."

Some of the biologists who have investigated pressure wave effects have referred to a "shock" wave, but if their biology is valid, I tend to be forgiving of imprecise language on the Physics side. It is never really clear in their papers whether they mean "shock wave" in the sense of a super-sonic compression wave or merely a pressure wave which creates a physiological "shock" effect.

This is why hydrostatic shock is a misnomer even if there may be some truth to the behavior. In fluid mechanical terms, it is neither hydrostatic nor a shock. The phenomenon itself may cause shock (as in the medical term), but that is something different.

I agree, hydrostatic shock is a misnomer. I only mentioned the term in the context of labels others have given to energy dependent effects.

There are other problems as well of course, for instance the wound mechanics of a broadhead arrow are almost completely different than those a handgun round. I realize you are trying to compare a projectile that creates a pressure wave (the bullet) to one that does not (the arrow).

Sure, but that merely means that the arrow observations do not provide conclusive proof of a pressure wave theory. It does not invalidate the observation as the basis of a hypothesis that would need more complete testing to be a theory.

While that is fine conceptually, any comparison of stopping power for a given wound size (as you do) is bound to be flawed because you lack a control variable.

Once again, your point would be valid if I referenced the arrow as proof of a theory rather than a basis for formulating a hypothesis. Experimental validation of a theory requires careful control variables. Formulation of a hypothesis does not.

There are more differences between an arrow wound and a bullet wound than just the presence of a pressure wave. Just the inclusion of the arrows shaft and how it alters bleeding changes things tremendously.

The arrow shaft almost always passes through completely on a deer hit broadside through the center of the chest. There may well be differences between an archery wound and a bullet wound, but the continuing presence of the arrow shaft altering bleeding is not one of them.

There are also problems with your "flaws." For instance many of Fackler's "flaws" are simply attempts to concentrate research on variables which can be adequately measured experimentally, like wound volume, bullet expansion, and penetration.

Variables like incapacitation can have large disparaties between individual test subjects and also require relatively expensive in vivo testing.

Without some correlation to actual effectiveness, all we have is the unproven presupposition and expert opinion that those gelatin measurements mean something.

But other than the M&S data set and the Strasbourg tests, are their any published data sets that allow for correlation between the easily measured variables like wound volume, bullet expansion, and penetration and a real measure of incapacitation?

Expert opinion is not the basis of science. Repeatable experiments are the basis of science. You really do not have to shoot a huge number of pigs, or goats, or deer to see whether or not easily measured variables like wound volume, bullet expansion, and penetration are better correlated to a real measure of incapacitation than pressure wave magnitude, energy dump, or TSC volume.

Yes, in vivo experiments are relatively expensive, but there needs to at least be enough in vivo experiments to determine which gelatin parameters are correlate the best with real measures of incapacitation.

Your post isn't bad work, but I really think it needs some revision.

I appreciate your comments, especially regarding the ambiguity of "sonic pressure wave" as used by Fackler and "shock wave" as used by Suneson et al. Given that there are at least two possible meanings for each term, what are the odds that the authors intend them to mean the same thing, as required for Fackler's criticism to not to be a straw man fallacy?

Michael Courtney

 

[Michael Courtney]

However, I've always put more faith in actual gunfight statistics than in gelatin. Given enough data, a trend will form, a mean will be established, and statistical variance can be calculated and analyzed for such data. At least THAT is something I can understand.

A trend does form, and we've found the trend in the data. Here's a quote from the draft of an article we're preparing for publication:

This article describes direct experimental evidence that incapacitation can be caused by a ballistic pressure wave independently from wounding caused by crushing effects of a bullet in the wound channel. Live mammals weighing 10-20 lbs were partially immersed in water and observed to be incapacitated by a ballistic pressure wave created by a bullet passing through the water close to the test subject without impacting the test subject. The water coupled the pressure wave to the thoracic cavity of the test subject without perforation. Handgun bullets producing larger pressure waves caused incapacitation, whereas bullets producing smaller pressure waves did not.

A second experiment provides experimental support for the veracity of the Strasbourg goat tests by using a similar experimental design observing incapacitation of whitetail deer by carefully controlled shot placement. Predictions based directly on the Strasbourg tests were validated in whitetail deer by showing that bullets of comparable wound channel volumes incapacitate much more quickly when a large ballistic pressure wave is present. Using comparable shot placement as the Strasbourg tests, one obtains an accurate prediction for the average incapacitation distance of deer by multiplying the Strasbourg average incapacitation time by the average death run speed of deer, 10 yards per second. This supports the Strasbourg results that reported a large pressure wave causing rapid incapacitation. (The Strasbourg tests used a high-speed pressure gauge inserted into the carotid artery.) Upon necropsy of the deer, we observe tissue damage due to the pressure wave for some bullets. This damage was remote from the wound channel and well beyond the range of the temporary stretch cavity.

We present time domain analysis of the Strasbourg test data showing that the probability of incapacitation depends on two independent mechanisms. One mechanism works quickly (< 5 seconds) and can be accurately modeled as a function of the ballistic pressure wave magnitude. The second mechanism works slowly (> 5 seconds) and is related to blood pressure drop from internal bleeding. The slow incapacitation mechanism depends on the quantity of tissue in which the bullet initiates bleeding. We believe the functional forms of our models are independent of species for mammals between 10 and 1000 lbs, with only two adjustable parameters being species specific.

Finally, this article presents an empirical model for predicting relative incapacitation probability in humans by employing the hypothesis that the wound channel and pressure wave effects each have an associated independent probability of incapacitation. Combining these two independent probabilities with the elementary rules of probability and performing a least-squares fit to the Marshall and Sanow data provides a empirical model with only two adjustable parameters for predicting “one shot stops” with a standard error of 5.5% and a correlation coefficient R = 0.939. The success of this model supports the hypothesis that wound channel and pressure wave effects are independent (within the experimental error), and it also allows assignment of the relative contribution of each effect for a given handgun load. This empirical model also gives the expected limiting behavior in the cases of very small and very large variables (wound channel and pressure wave), as well as for incapacitation by rifle and shotgun projectiles.

Michael Courtney

 

[MCgunner]

Excellent! So the Marshall/Sanow data correlates statistically with your theories of probability of incapacitation! Wow, I hope when you're through with this paper, it'll be on the net somewhere in total. I don't know if I'll understand all of it, but it sure would be worth reading!

So, then, you can actually MODEL the incapacitation probability of a given load? What would be the variables you'd need for the model? Or, is that way too complicated for a BBS thread? LOL!

Not that I'm that knowledgeable, but this surely sounds like break though stuff to me. I've always suspected just what you are postulating here, just didn't know enough about what I was theorizing. I likened the pressure wave to a sonic boom effect or something of that nature and often thought there might be something magical about a bullet velocity exceeding the speed of sound. What I was sure of is there was some mechanism of energy transfer there that was more than just lead crushing flesh. I can see that from my hunting experience.

 

[Bobo]

I'll leave the rhetoric to those with the skills.

All I can say is - Great Stuff!!

Thanks for sharing.

 

[ghost squire]

Someone once said that academic debates are often vicious because the stakes are so small (or something along the lines of that). In my opinion even if anyone ends up proving anything on this forum (hasn't been done on the internet in oh... ever) what will it end up accomplishing? People have been hit with 25mm Bushmaster cannons and survived, .50 BMGs, survived an unholy array of explosives and shrapnel, survived 20 rounds to the chest of 9mm...

I can tell you right now that an ammunition manufacturer will find some way to twist your words to market his BS novelty ammunition, perfect for unobstructed lung shots on alpine goats from a set distance away and with no barriers.

The fact is there are many variables in this sort of thing. When you use a bullet thats velocity and construction dependant (for wounding effects), Murphys law dictates that you're going to have to fire it from a half kilometer away and it will clog in the guys 10 wool coats. I have less and less doubt that the Strasbourg tests happened as time goes on. But at the end of the documentation of these tests, it even says that they should be taken as they are and not out of context, they are tests determining what type of handgun cartridge is most efficient at killing alpine goats with unobstructed lung shots. The bullets do not pass through the heart, they do not have to penetrate a winter jacket, a denim vest and 3 other layers of clothing plus 5 inches of fat and then the sternum.

Then there are variables to think about besides the terminal ballistics themselves. Cost of ammunition, the more it costs the less you practice. Flash and noise, many of the handgun calibers that start touching the rifle threshold of wounding effects (10mm etc) have excessive amounts of it, so much so that firing them at night would instantly blind you. Excessive flash, noise and recoil might cause flinching. Excessive noise might damage hearing more then another caliber might, lowering situational awareness.

Facklers writings are the standard pillar of wisdom in the world of wound ballistics simply because you can peck away at it, but you can never topple it. What he says as a whole ends up being proven true time and time again.

 

[Michael Courtney]

Excellent! So the Marshall/Sanow data correlates statistically with your theories of probability of incapacitation! Wow, I hope when you're through with this paper, it'll be on the net somewhere in total. I don't know if I'll understand all of it, but it sure would be worth reading!

So, then, you can actually MODEL the incapacitation probability of a given load? What would be the variables you'd need for the model?

The independent variables are the magnitude of the pressure wave and the size of the permanent crush cavity.

Not that I'm that knowledgeable, but this surely sounds like break though stuff to me. I've always suspected just what you are postulating here, just didn't know enough about what I was theorizing.

"Break through" might be an overly-optimistic choice of words. We think we've done interesting and useful science that has potential application to bullet design and selection.

I likened the pressure wave to a sonic boom effect or something of that nature and often thought there might be something magical about a bullet velocity exceeding the speed of sound.

Here's where the science deviates from some of the common perceptions. There is no magic bullet. There is not a velocity where the pressure wave effect "turns on" suddenly. The pressure wave effect turns on gradually, and depends on peak pressure wave magnitude, not on velocity.

What I was sure of is there was some mechanism of energy transfer there that was more than just lead crushing flesh. I can see that from my hunting experience.

We had hunting experiences similar to yours which helped lay the groundwork for the formulation of the pressure wave hypothesis. Together with the peer-reviewed research referenced in the initial post of this thread, we though we had a hypothesis worth more careful testing.

The trouble at this point was the lack of published data that inspired confidence. The anonymity of the Strasbourg tests and negative views of the M&S data set gave us pause. Consequently, we designed the deer experiment to test the hypothesis that Strasbourg was a wholesale fraud, and we found a 90% confidence level that the Strasbourg average incapacitation times are reliable.

We also gave careful consideration to the criticisms of the M&S data set and we concluded that many of the criticisms are exaggerated, and where there are some valid criticisms, these impact only the accuracy of interpreting the OSS rating as a relative measure of bullet effectiveness. Together with the fact that the OSS ratings are highly correlated with the Strasbourg test average incapacitation times (which we experimentally showed are not fraudulent), we had enough confidence to develop a model with the M&S OSS data set.

It is notable that both the Strasbourg authors and Marshall and Sanow were suggesting a pressure wave mechanism 14 years ago, and in the time since then, the field of neurology has shown that a pressure wave applied directly to the brain can cause both incapacitation and neural injury. All we've done is connect the dots.

Michael Courtney

 

[MCgunner]

Someone once said that academic debates are often vicious because the stakes are so small (or something along the lines of that). In my opinion even if anyone ends up proving anything on this forum (hasn't been done on the internet in oh... ever) what will it end up accomplishing? People have been hit with 25mm Bushmaster cannons and survived, .50 BMGs, survived an unholy array of explosives and shrapnel, survived 20 rounds to the chest of 9mm...

I can tell you right now that an ammunition manufacturer will find some way to twist your words to market his BS novelty ammunition, perfect for unobstructed lung shots on alpine goats from a set distance away and with no barriers.

The fact is there are many variables in this sort of thing. When you use a bullet thats velocity and construction dependant (for wounding effects), Murphys law dictates that you're going to have to fire it from a half kilometer away and it will clog in the guys 10 wool coats. I have less and less doubt that the Strasbourg tests happened as time goes on. But at the end of the documentation of these tests, it even says that they should be taken as they are and not out of context, they are tests determining what type of handgun cartridge is most efficient at killing alpine goats with unobstructed lung shots. The bullets do not pass through the heart, they do not have to penetrate a winter jacket, a denim vest and 3 other layers of clothing plus 5 inches of fat and then the sternum.

Then there are variables to think about besides the terminal ballistics themselves. Cost of ammunition, the more it costs the less you practice. Flash and noise, many of the handgun calibers that start touching the rifle threshold of wounding effects (10mm etc) have excessive amounts of it, so much so that firing them at night would instantly blind you. Excessive flash, noise and recoil might cause flinching. Excessive noise might damage hearing more then another caliber might, lowering situational awareness.

Facklers writings are the standard pillar of wisdom in the world of wound ballistics simply because you can peck away at it, but you can never topple it. What he says as a whole ends up being proven true time and time again.

You don't find it even remotely interesting????

Fackler's "wisdom"? His drivel has only been around a decade or two. It was once wisdom that the earth was flat and they burned folks at the stake that didn't believe it and spoke out against it. Of course, terminal ballistics discussions aren't nearly as important, but hey, it still interests me and, unlike Fackler, this actually makes sense to me.