Restraint Asphyxiation

While training in the Mandt System for work, I was introduced to a phenomenom of restraint asphyxiation where an increase of neuro-transmitters known as catecholamines can lead to a heart attack anytime upto 24 hours after being restrained.

One of the sources quote was Restraint Asphyxia - Silent Killer by Charly D. Miller, Paramedic EMS Author & Educator, and Consultant Restraint Asphyxia Expert Witness. I find all the text emphasizing more than a little distracting. So here is the section, I wish to concentrate on:

States of extreme emotional- and physical-exertion also generate excessive
production of several other naturallyproduced body chemicals; especially the
chemicals released by the "Fight/Flight" nervous system, such as adrenalin and
noradrenalin. Medical professionals call these naturally-produced "Fight/Flight"
chemicals, "catecholamines." During all of the emotionally- and
physicallyexertive activities that precede and are associated with restraint
asphyxia deaths, progressively-increasing amounts of catecholamines are released
into the Victim's system.

This creates what medical professionals call a, "hypercatabolic state" – an
"overdose" of these naturally-produced chemicals. A hypercatabolic state is a
chemical imbalance that weakens ALL of the body's muscles. But, it especially
weakens the respiratory muscles.(1,12)

A hypercatabolic state also adversely effects the HEART.(1,12)

Catecholamines cause the heart to contract (beat) faster, and with greater FORCE of contraction – exerting greater "effort" to work. Since the heart is a muscle that (like the respiratory muscles) is entirely unaccustomed to having to work terrifically hard for a prolonged period of time, the heart rapidly becomes exhausted when required to work harder than it is used to working. Furthermore; to work FASTER and more FORCEFULLY, the heart muscle requires more SUGAR and OXYGEN to fuel an increased functional performance demand.

But, when struggling against Restrainers, the Victim's extremity muscles are using up the vast majority of the body's sugar stores. So, less and less sugar is available to fuel the heart's function. AND, when struggling against Restrainers, the Victim's heart requires greater than "normal" amounts of oxygen to support the increased workload that is demanded of it. BUT, if the Victim is struggling against Restrainers who are employing a form of restraint that MAKES BREATHING DIFFICULT (such as forceful-prone-restraint), his heart receives far less than normal amounts of oxygen.(1,17,26-28,40)

The Canadian Journal of Psychiatry June 2003 has this article on the subject. The following snippet talks about Catecholamine Rush:

Massive release of adrenal catecholamines may occur in patients who are involved
in escalating agitation, struggles with staff members, and “takedowns” to the
ground or who are carried elsewhere and secured with restraints. This
catecholamine outpouring may sensitize the heart and produce rhythm disturbances
(23). Behavioural arousal and psychological stress have been shown to induce
malignant cardiac rhythm disturbances (23–25).
Neural and psychological factors have been implicated as risk factors for ventricular arrhythmias and sudden death (24–26). Neural integration of body functions takes place through a complex system of feedback loops when information from within and without the organism is taken in and catalogued by the brain. These pathways play a major role in causing sudden death in persons who find themselves in perilous
situations. Moreover, the situations need not be perilous to precipitate cardiac
arrhythmias (26). Lown and colleagues identified psychic stress as a mediating
factor for advanced cardiac arrhythmias, and it has been suggested that
emotional extremes are triggering mechanisms for sudden cardiac death (24–26).
Deaths associated with extreme physiological exertion differ somewhat.
Emergency medicine physicians recently reported cases of profound metabolic
acidosis in cardiac arrest associated with use of restraints. In a sample of
patients who died—most, but not all of whom had been under the influence of
cocaine—the recorded blood pH was 6.25. The common variable was extreme exertion from either fleeing or fighting vigorously while being subdued. The authors
speculate that psychosis and delirium, including drug-induced delirium, alter
pain sensation and may thus render patients capable of exertion far beyond their
normal capacity, leading to maximal sympathetic discharge and catecholamine
depletion (27). By provoking further struggle, physical restraint results in
overwhelming acidosis. Acidosis of this magnitude should trigger physiologic
compensatory mechanisms, but the prone restraint position may limit reflex
compensation (27).

Another article has information on it, but I would have to subscribe to read it:
Weight Force During Prone Restraint and Respiratory Function.
American Journal of Forensic Medicine & Pathology. 25(3):185-189, September 2004.Chan, Theodore C. MD *; Neuman, Tom MD *+; Clausen, Jack MD +; Eisele, John MD ++; Vilke, Gary M. MD *

Actually there are several other articles similarly protected.

Researching "Catecholamine Rush", I found a nice little article on the Science Blog, reprinted from Columbia University College of Physicians and Surgeons:

The more calcium that the ryanodine receptor releases, the stronger the
contraction of the heart. Dr. Marks and his colleagues have discovered that
increased levels of catecholamines, chemicals such as adrenaline that help
transmit nerve impulses, can trigger the ryanodine receptor to release more
calcium.
Patients with heart failure have high levels of catecholamines in
their blood, but their calcium ion release system does not respond properly to
these neurotransmitters. This causes the nervous system to release even more
catecholamines, with little or no response from the heart muscle. Dr. Marks
discovered that a malfunctioning ryanodine receptor is the weak link in the
calcium channel release system that causes this failure in catecholamine
response.