The dangerous pressure points knockout effect on death point Stomach 9 is one aspect of dim mak that has been abused by many unqualified pressure point teachers of the martial arts, causing the victim (a volunteer) to fall unconscious. This point unnecessarily traumatises the carotid artery which can lead to serious and urgent medical attention, either at the time of impact or in the future. The truth is that there are many other vital points that give the knockout effect.
In our dim mak classes and seminars with Grandmaster Dr Pier Tsui-Po, we do not knockout each other during training or during demonstrations. He teaches to all his students how to apply this knockout technique. More importantly, he teaches the mechanisms of the knockout, both in the Chinese and Western medical sciences, and he teaches all the other pressure points that can cause a knockout effect. You'll be surprised to know that there are many other points on the body that give the knockout effect.
In helping you understand the dangers of hitting dim mak death point Stomach 9 to achieve a knockout effect and cause unnecessary damage to the carotid artery of the neck, here are some information on the dim mak knockout as taught by Grandmaster Tsui-Po.
Direct trauma to the head can cause loss of consciousness through disruption of brain function, but the head is well-protected. An alternative is to attack peripheral structures that can cause fainting through the vasovagal nerve reflex of the nervous system.
Vasovagal fainting occurs when the part of the nervous system that regulates heart rate and blood pressure malfunctions in response to a trigger, such as pain. The heart rate slows, and the blood vessels in the legs widen. This allows blood to pool in the legs, which lowers blood pressure. This drop in blood pressure and slowed heart rate quickly cause diminished blood flow to the brain, and consequent fainting. Autonomic symptoms may precede this. Classically, nausea, sweating, fading or "graying out" of vision, stomach discomfort, and light-headedness precede fainting by a few minutes.
Neurocardiovascular Regulation of Blood Pressure
Fainting occurs due to a drop in blood flow to the brain. Brain tissue depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic energy source. Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body; therefore, a cessation of blood flow lasting only 3-5 seconds results in fainting. Brain blood flow is maintained relatively constant by an intricate and complex feedback system involving cardiac output, blood vessel resistance, arterial pressure, blood volume and metabolic regulation. A significant defect in any one of these or mild defects in several of these systems may cause fainting.
Physiologic control of blood pressure regulation involves complex nerve input signal processing by the central nervous system and subsequent nerve output signals to the heart and blood vessel targets. Normal moment-to-moment regulation of arterial pressure is controlled predominantly by stretch-activated baroreceptors (pressure sensors) located in the major blood vessels to the brain. The nerve input signals are transmitted from the aortic arch by the vagus nerve and from the carotid sinus by the glossopharyngeal nerve. Distention of the blood vessels here after heart contraction results in discharge of input nerves that converge on the brain stem. At this site, sympathetic nerve outflow is reduced and vagal nerve outflow is increased.
If there is a decrease in the level of arterial pressure, the mean level of sympathetic outflow increases and vagal outflow decreases. Likewise, increases in arterial pressure result in sympathetic nerve activity drop and vagal nerve activity increase. Consquently, the arterial baroreceptor system regulates the beat-to-beat firing of sympathetic and vagal nerves. Mean levels of sympathetic nerve outflow are also regulated by low-pressure baroreceptors located in the heart walls and blood vessels in the chest(so-called cardiopulmonary baroreceptors). Increased blood flow to the heart activate these receptors, resulting in sympathetic inhibition. Conversely, decreased blood flow to the heart cause sympathetic excitation because these receptors decrease their firing rate.
Additional Mechanisms of Vasovagal Response
Vasovagal fainting in humans, however, is also triggered by other mechanisms. Similar pressure receptors are also present in other parts of the body such as the bladder, rectum, oesophagus and lungs. So, other triggers to reflex vasovagal fainting include prolonged toilet straining at urination or defaecation, difficulty swallowing and coughing fits. Also conscious input responses in the higher central nervous system have also been implicated. For example, during emotional stress, input signals from the forebrain and hypothalamus can also play a role.
Common triggers for vasovagal fainting include:
The origin of vasovagal syncope is probably as an evolutionary trait to protect the heart or to escape predators. In animals, fear and threat bradycardia occur with the heart rate slowing, and the vasovagal fainting reflex also occurs during heavy blood loss in hemorrhagic shock in humans and animals. This suggests that vasovagal syncope evolved as an advantageous response to inescapable predators or to stressful and possibly dangerous heart conditions.
The inhibition of the sympathetic system, together with activation of the vagal system, characterizes vasovagal fainting. The consequent slowing of the heart rate induced by the vasovagal fainting reflex may constitute a beneficial break for the heart pump, thereby reducing heart muscle oxygen consumption and may also allow the simulation of death - i.e. playing possum.
Other things that will cause this low blood pressure are sudden intense stimulation of pain receptors in such body organs as the gall bladder, small and large intestines, kidneys and ureters (the drainage tubes between the kidneys and bladder). A dim mak pressure point attack to these abdominal organs can also cause the vasovagal response with fainting.
Now all these major abdominal organs have meridians with their own line of acupuncture points across different parts of the body. Striking any one of these points causes the body to think that the actual organ has been struck. So, for example, striking Colon 10 on the upper forearm can cause overstimulation and damage to the colon and trigger an indirect fainting through colonic stimulation initiating vasovagal fainting. Also, Colon 10 is located on the superficial branch of the Radial Nerve and a vasovagal faint can be caused by the intense pain of a nerve strike here. These mechanisms are not mutually exclusive and both can act together for extra effect.
All the various pressure points that cause knockout effect are detailed in the Dim Mak Manual - Art and Science of deadly pressure point fighting.
Other courses such as the Ghost Hands of dim mak also present a variety of these knockout points.
Grandmaster Tsui-Po also teaches special intensive seminars on the theory and applications of all dim mak knockout points.
A Final Word of Caution
Please be very careful. Learn the art of dim mak properly, and from a "real" pressure point expert because some of these points are either lethal or can cause serious injury or harm, either at the time of impact or at a later date.
Thanks to Dr Michael Croce for this contribution. Michael is a devoted dim mak and kung fu student of Grandmaster Tsui-Po's Dim Mak World Golden Lion Academy..
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