From: jaybob@crl.com (Jay Wiseman) / Newsgroups: alt.sex.bondage Subject: Re: Breath Control / Date: 30 Dec 1995 11:05:17 / Message-ID: (4c42hd$ib@crl3.crl.com)
This is one of the most controversial aspects of BDSM. It has been debated and argued about until all concerned were "blue in the face" on many occasions here. The following is a (slightly edited) version of an article I wrote about it. I hope you find it at least somewhat helpful.
Regards,
Jay
The Medical Risks of Breath Control Play
by Jay WisemanU Author of "SM 101: A Realistic Introduction"U
For some time now, I have felt that the practices of suffocation and/or strangulation done in an erotic context (and generically known as breath control play) were in fact far more dangerous than they are generally perceived to be. As a person with years of medical education and experience, I know of no way whatsoever that either suffocation or strangulation can be done in a way that does not intrinsically put the recipient at risk of cardiac arrest. (There are also numerous additional risks; more on them later.) Furthermore, and my biggest concern, I know of no reliable way to tell when such a cardiac arrest becomes imminent.
Often the first detectable sign that an arrest is approaching is the arrest itself. Furthermore, if the recipient does arrest, the probability of resuscitating them, even with optimal CPR, is distinctly small. Thus the recipient is dead and their partner, if any, is in a very perilous legal situation (the authorities consider such deaths first-degree murders until proven otherwise, with the burden of such proof being on the defendant). There is also the real and major concern of the surviving partner's own life-long emotional reaction to having caused such a death, plus the reactions of the friends and family members of both parties.
I have discussed my concerns regarding breath control with well over a dozen SM-positive physicians, and with numerous other SM-positive health professionals, and all share my concerns. We have discussed how breath control might be done in a way that is not life-threatening, and come up blank. We have discussed how the risk might be significantly reduced, and come up blank. We have discussed how it might be determined that an arrest is imminent, and come up blank.
Indeed, so far not one (repeat, not one) single physician, nurse, paramedic, chiropractor, physiologist, or other person with substantial training in how a human body works has been willing to step forth and teach a form of breath control play that they are willing to assert is acceptably safe -- i.e., does not put the recipient at imminent risk of dying. I believe this fact makes a major statement.
Other "edge play" topics such as suspension bondage, electricity play, cutting, piercing, branding, enemas, water sports, and scat play can and have been taught with reasonable safety, but not breath control play. Indeed, it seems that the more somebody knows about how a human body works, the more likely they are to caution people about how dangerous breath control is, and about how little can be done to reduce the degree of risk.
In many ways, oxygen is to the human body, and particularly to the heart and brain, what oil is to a car's engine. Indeed, there's a medical adage that goes "hypoxia (becoming dangerously low on oxygen) not only stops the motor, but also wrecks the engine." Therefore, asking how one can play with breath control is very similar to asking how one can drive a car while draining it of oil. Some people tell the "mechanics" something like, "Well, I'm going to drain my car of oil anyway, and I'm not going to keep track of how low the oil level is getting while I'm driving it, so tell me how to do this with as much safety as possible" and then get frustrated when the "mechanics" scratch their heads and say that they don't know.
A bit about my background may help explain my concerns. I was an ambulance crewman for over eight years. I attended medical school for three years, and passed my four-year boards, (then ran out of money). I am a former member of the American Academy of Family Physicians and a former American Heart Association instructor in Advanced Cardiac Life Support. I also have an extensive martial arts background (first-degree black belt in Tae Kwon Do), including several months of judo training that involved both choking and being choked, and have participated in training seminars for police officers. Finally, I have been an instructor in first aid, CPR, and advanced emergency care for over fifteen years. I currently offer first aid and CPR training to the SM community.
During my ambulance days, I responded to at least one call involving the death of a young teenage boy who died this way, and to several other calls where this was suspected but could not be confirmed. Additionally, I personally know two members of the local SM community who went to prison after their partners died during breath control play.
The primary danger of breath control play is that it is not a condition that gets worse over time (regarding the heart, anyway, it does get worse over time regarding the brain). Rather, what happens is that the more the play is prolonged, the greater the odds that a cardiac arrest will occur.
Quick physiology lesson: Then the heart gets low on oxygen, it starts to fire off "extra" pacemaker sites. These usually appear in the ventricles and are thus called premature ventricular contractions -- PVC's for short. If a PVC happens to fire off during the electrical repolarization phase of cardiac contraction (the dreaded "PVC on T" phenomenon) it can kick the heart over into ventricular fibrillation -- a form of cardiac arrest. The lower the heart gets on oxygen, the more PVC's it generates, thus increasing the probability of a PVC-on-T and resultant cardiac arrest.
When this will happen to a particular person in a particular session is just simply not predictable. This is exactly where most of the medical folks I have discussed this topic with "hit the wall." The question quickly becomes: How are you gonna know when they start throwing PVC's? The basic answer is: You basically can't.
Past experience, either with others or with that same person, is not particularly useful. Carefully watching their level of consciousness, skin color, and pulse rate is of only limited value. Even hooking them up to both a pulse oximeter and a cardiac monitor would be of only limited additional value. (If you had them hooked to a cardiac monitor you could tell when they start throwing PVC's. The problem is that each PVC is like a bullet whizzing past, and even if you "ease up" on the bottom immediately there's no telling when the PVC's will cease appearing.)
What is certain is that the "danger zone" is reached fairly quickly. Forensic pathology texts document cardiac arrests from as little as one minute of suffocation and as little as a few seconds of strangulation.
In addition to this primary danger, there are many documented secondary dangers. These include, but are _not_ limited to: rupture of the windpipe, fracture of the larynx, damage to the blood vessels in the neck, dislodging a fatty plaque in the neck arteries which then travels to the brain and causes a stroke, damage to the cervical spine, seizures, airway obstruction by the tongue, and aspiration of vomitus. Additionally, there are documented cases in which the recipient appeared to fully recover but was found dead several hours later.
The American Psychiatric Association estimates a death rate of one person per year per million of population -- thus about 250 deaths last year in the U.S. Law enforcement estimates go as much as four times higher. Most such deaths occur during solo play, however there are many documented cases of deaths that occurred during play with a partner. It should be noted that the presence of a partner does nothing to limit the primary danger, and does little or nothing to limit most of the secondary dangers.
Many people teach that choking can be safely done if pressure on the windpipe is avoided. Their belief is that pressing on the arteries leading to the brain can safely cause unconsciousness. The reality, unfortunately, is that pressing on the carotid arteries, _exactly_ as they recommend, presses on baroreceptors known as the carotid sinus bodies. These bodies then cause vasodilation in the brain, thus there is not enough blood to perfuse the brain and the recipient loses consciousness.
Unfortunately, in addition to this, a message is also sent to the main pacemaker of the heart, via the vagus nerve, to decrease the rate and force of the heartbeat. Most of the time, under strong vagal influence, the rate and force of the heartbeat is reduced by one third. However, every now and then, the rate and force is decreased to zero and the bottom "flatlines" into asystole -- another, and more difficult to cope with, form of cardiac arrest. There is no way to tell whether or not this will happen in any particular instance.
For the reason cited above, many police departments have now either entirely banned the use of choke holds or have reclassified them as a form of deadly force. Indeed, a local CHP officer recently had a $250,000 judgment brought against him after a nonviolent suspect died while being choked by him.
Finally, as a CPR instructor myself, I want to caution that knowing CPR does little to make the risk of death from breath control play significantly smaller. While CPR can and should be done, understand that the probability of success is likely to be less than 10%.
I'm not going to state that breath control is something that nobody should ever do under any circumstances. Informed people can take any degree of risk they wish. I am going to state that there is a great deal of ignorance regarding what actually happens to a body when it's suffocated or strangled, and that the actual degree of risk associated with these practices is far greater than most people believe.
I have noticed that, when people are educated regarding the severity and unpredictability of the risks, fewer and fewer choose to play in this area, and those who do continue tend to play less often. I also notice that, because of severe and unpredictable risks, more and more SM party-givers are banning any form of breath control play at their events.
If you'd like to look into this matter further, here are some references to get you started:
"Medical Physiology" by Guyton
"Emergency Care in the Streets" by Caroline
"The Pathologic Basis of Disease" by Robbins
"Autoerotic Fatalities" by Hazelwood
Journal of Forensic Sciences
People with questions or comments can contact me at jaybob@crl.com or write to me at P.O. Box 1261, Berkeley, CA 94701.
Regards,
Jay
*******************
From: jaybob@crl.com (Jay Wiseman) / Newsgroups: alt.sex.bondage Subject: Breath control cumulative brain damage / Date: 5 Jan 1996 / Message-ID: (4cjq0g$3ri@crl2.crl.com)
As has been prominently pointed out, in my latest post regarding the risks of breath control play I mentioned a concern that I had not raised in my previous posts: That there is hypoxia-induced _cumulative_ brain damage associated with strangulation and/or suffocation even if no major primary complication, such as cardiac arrest, or secondary complication, such as a seizure, occurs. Several people, understandably, asked me how I "really knew" that cumulative damage took place.
Well, truth be told, I didn't, directly, know that it was true. I *did* have pretty good reason to believe that it was true. After all, two M.D. Neurologists and a PhD Neurophysiologist had told me that cumulative damage occurred. Also, another SM friend had told me that he had been told by an Anesthesiologist that it occurred. So I had been advised, either directly or indirectly, by no fewer than four people with extensive professional training in how the nervous system functioned that cumulative damage occurred secondary to episodes of cerebral hypo-oxygenation.
Additionally, I knew that brain cells died if (among many other causes) the blood nourishing them got too low on sugar, or if its pH got too low or too high, or if there was physical trauma to them. (It's been known for ages that the blows to the head that take place in boxing, in addition to occasionally causing a fatal intra-cranial hemorrhage, kill neurons in goodly numbers.)
That was good enough for me, but was it good enough for a.s.b.? Har!
Still, the requests for documentation were not unreasonable, and I can see a world-class medical school from my bedroom window, so I got myself over to its library and spent the better part of a day searching for verifiable, scientific-quality, information to support or (God forbid!) refute my claim. It was, after all, possible that all four of these professionals had been wrong and I would have to issue a craven apology and retraction.
Well, thanks to a MEDLINE search on the keywords "cumulative cerebral ischemia," it didn't take me long to get several "hits." I photocopied the three that seemed the most relevant, and have summarized them below. Any comments of my own are contained within [].
Journal article # 1
"Judo as a possible cause of anoxic brain damage; A case report", by Owens and Ghandiali
The Journal of Sports Medicine and Physical Fitness, December 1991
Abstract: The rules of judo provide for strangulation techniques in which the blood supply to the brain is blocked by pressure on the carotid arteries; such techniques produce anoxia and possible unconsciousness if the victim fails to submit. A case is presented of a patient with signs of anoxic brain damage, with psychometric investigations showing memory disturbance consistent with a left temporal lobe lesion. This patient had been frequently strangled during his career as a judo player; it is suggested that such frequent strangulation was the cause of the damage. Such an observation indicates the need for caution in the use of such techniques.
A few quotes from the article:
"The patient was a 33-year-old male international class judo expert who was admitted as an emergency following a sudden loss of consciousness followed by definite left hemiparesis, confusion, and amnesia. Power returned quickly to the left arm and leg but his memory remained poor; during the six weeks prior to his admission he had apparently suffered episodes of altered awareness and occasional loss of consciousness. Skull X-ray was normal and a subsequent CAT scan revealed no evidence of abnormality. He was discharged with a diagnosis of suspected anoxic brain damage but following repeated fainting episodes and persisting difficulties with memory over the following months, he returned for further assessment."
"It was concluded that anoxia resulting from his judo experiences had resulted in the lesion and he was discharged with instructions to cease his participation in the sport."
"Anoxic brain damage is not a common form of sports injury but the unique characteristics of judo suggest that under certain circumstances a picture similar to that defined here may result from participation."
"In addition it should be noted that judo players are commonly strangled into unconsciousness during teaching either as an illustration of the effectiveness of the technique or in order to demonstrate the judo resuscitation procedures ("kuatsu"). Such circumstances do not, as far as we are aware, occur in any other sport. The present case had apparently been frequently strangled into unconsciousness during his judo career and it was surmised that the cumulative effect of such strangulation had been, at least in part, the cause of the anoxic brain damage. Whilst it is of course possible that some other factor was responsible, there was nothing in his detailed case history other than the judo to account for the sustained anoxia, which is of course rarely seen in a patient of such age. It may be appropriate therefore to recommend caution to judo players regarding such techniques."
Journal article # 2
"Neuronal damage following repeated brief ischemia in the gerbil", by Kato, Kogure, and Nakano. Brain Research, 479 (1989)
Abstract: The effect of repetition of brief ischemia, which causes no morphological brain damage when given as a single insult, was studied. Two-minute forebrain ischemia was induced in gerbils singly and three or five times at 60-minute intervals. Although [a single incident of] two-minute ischemia induced no neuronal damage, three or five repeated ischemic insults caused neuronal damage in the selectively vulnerable regions, the severity being dependent on the number of episodes.
A few quotes from the article:
"Gerbils subjected to a single two-minute ischemia (n=5) revealed no abnormal calcium accumulation throughout the brain. In all animals subjected to three two-minute ischemic insults (n=5), abnormal calcium accumulation was shown in the CA1 sector of the hippocampus and the thalamus; there was also such abnormal calcium accumulation in the dorsolateral part of the striatum and the substantia nigra in 8 of 10 hemispheres, and in the inferior colliculus in 2 of 10 hemispheres. Gerbils subjected to five two-minute ischemic insults (n=4) revealed most severe calcium accumulation in the brain."
"Abnormal calcium accumulation shown by 45Ca-autoradiography has been reported to be equivalent to the sites of neuronal damage and is a useful tool for mapping the distribution."
"Gerbils subjected to a single two-minute ischemia (n=5) showed no neuronal damage throughout the brain. In animals killed four days after three 2-minute occlusions (n=4) the CA1 neurons had disappeared in all animals. Various degrees of neuronal injury were seen in the striatum and thalamus. In animals subjected to five 2-minute occlusions, the changes were generally more pronounced than in animals subjected to three 2-minute occlusions."
"The present study indicates that repeated ischemia causes brain injury depending on the number of episodes, even though no morphological brain damage results when the ischemia is induced as a single insult."
Journal article # 3
"Neuronal damage and calcium accumulation following repeated brief cerebral ischemia in the gerbil", by Araki, Kato, and Kogure
Brain Research (528) 1990
Abstract: [The abstract was presented as a single very long paragraph; I've broken it into several shorter paragraphs to improve readability.]
We investigated the distribution of neuronal damage following brief cerebral transient ischemia and repeated ischemia at one-hour intervals in the gerbil, using light microscopy and 45Ca-autoradiography as a marker for detection of ischemic damage. The animals were allowed to survive for seven days after ischemia induced by bilateral carotid artery occlusion.
Following [a single instance of] two-minute ischemia, neuronal damage determined by abnormal calcium accumulation was not observed in the forebrain regions. Following [a single instance of] three-minute ischemia, however, abnormal calcium accumulation was recognized only in the hippocampal CA1 sector and part of the striatum.
Two 2-minute ischemic insults caused extensive abnormal calcium accumulation in the dorsolateral part of the striatum, the hippocampal CA1 sector, the thalamus, the substantia nigra, and the inferior colliculus. The ischemic results were more severe than that of a single three-minute ischemia. However, three 1-minute ischemic insults caused abnormal calcium accumulation only in the striatum. On the other hand, three 2-minute ischemic insults caused severe abnormal calcium accumulation in the brain. The abnormal accumulation was found in the dorsolateral part of the striatum, the hippocampal CA1 sector, the thalamus, the medial geniculate body, the substantia nigra, and the inferior colliculus. Gerbils subjected to three 3-minute ischemic insults revealed the most severe abnormal calcium accumulation.
Marked calcium accumulation was seen not only in the above sites, but also spread in the neocortex, the septum, and the hippocampal CA3 sector. Morphological study after transient or repeated ischemia indicated that the distribution and frequency of the neuronal damage was found in sites corresponding to most of the regions of abnormal calcium accumulation. The abnormal calcium accumulation, however, was not only found in the regions such as the neocortex and the hippocampal CA3 sector where the neuronal damage was seen.
The present study demonstrates that repeated ischemic insults at one-hour intervals can produce severe neuronal damage not only in the basal ganglia and the limbic system, but also in the brainstem. Furthermore, they suggest that the cumulative effects after repeated ischemic insults are related to the time of the ischemia or the number of episodes.
A few quotes from the article:
"The present study has demonstrated that brief but repeated forebrain ischemia in the gerbil can cause severe neuronal damage not only in the basal ganglia and the limbic system, but also in the brainstem."
"It is well known that certain regions such as the neocortex, hippocampus, striatum, thalamus, and cerebellum are selectively vulnerable. The present study also suggests that repeated ischemic insults can produce severe neuronal damage in selectively vulnerable regions when it is induced repeatedly at one-hour intervals. These patterns of neuronal damage after repeated ischemia are essentially the same as those following a single 10-15 minute ischemia in the gerbil, and the mechanisms of ischemic neuronal damage in repeated ischemia are partly the same as those in transient ischemia."
"The neuronal injury of the brainstem, therefore, may be due to excessive lactic acid accumulation."
"In conclusion, the present study indicates that repeated brief ischemic insults can cause severe neuronal damage not only in the basal ganglia and the limbic system but also in the brainstem. Furthermore, they suggest that the cumulative effect after repeated ischemic insults is related to the time of the ischemia and the number of episodes."
xxxxxxxxxx End of journal material xxxxxxxxxx
Please, folks, no gerbil jokes.
Regards,
Jay