Excerpts From Dr. Bernard Knight's Writings
What follows below are some of the more relevant excerpts from the textbook writings ("Forensic Pathology" 3rd edition) of British forensic pathologist
Dr. Bernard Knight. They address the question of rapid and sudden cardiac arrest caused by vagus nerve stimulation of the heart. Let me observe that
Chapter 15, "Fatal Pressure On The Neck" is the most intensive and detailed treatment of this particular topic that I have ever found in the medical
literature. This information is provided as part of a long-ongoing debate as to the riskiness of engaging in "breath control games" with one's partner
during erotic play. Just to mention it, I'm a court-qualified expert witness in erotic asphyxiation and have done work in several homicide cases, including
two death penalty cases, in which
this question was at issue.
At least for now (07/08/10) chapters 14 and 15 can be read in their entirety here: http://kinks.ca/wiki/index.php?title=Knight%27s_forensic_pathology_pdf.
Potential viewers should be advised that the material contains numerous fairly grisly photographs. Those with a weak stomach should brace themselves
accordingly.
Vagal-induced causes of sudden cardiac arrest.
From chapter 14: "Asphyxia"
By suffocation secondary to sudden exposure to increased concentrations of carbon dioxide.
(Starting on page 357)
"Although safety precautions demand venting before the men enter, some workers still suffer a sudden death upon encountering an atmosphere rich in carbon
dioxide...In all of these deaths associated with replace oxygen with an inert gas, rapid death is common before hypoxia can have had any physiological
effect. For example, the author (BK) has dealt with two deaths in which seafarers entered closed ships' tanks and virtually fell dead off the empty
ladder. The presumed mechanism, which was far too quick to be hypoxic, was considered to be some overstimulation of the chemoreceptor system, leading to
a parasympathetic "vasovagal" cardiac arrest.
By plastic bag suffocation. (Page 359)
"Plastic bag suffocation can be rapid and leave no signs whatsoever...As with hypoxic atmospheres, it seems that the mechanism of death is some rapid
cardio-inhibitory mode, rather than a hypoxic process."
By choking (here meaning: as in by choking on a piece of food) (Page 361)
"Death can be the result of pure hypoxia by occlusion of the airway...As described below, however, a large proportion of deaths occur suddenly before any
possible hypoxic manifestations have had time to take effect; these fatalities must be caused by a neurogenic cardiac arrest; either purely neurogenic or
accelerated by excessive catecholamine release from the adrenaline response."
Continuing discussion of sudden death from choking on food (page 362)
"The most frequent victims were well-nourished businessmen, who died suddenly and unexpectedly during a meal, with no signs of respiratory distress or any
of the 'classic signs of asphyxia.' Initially thought to be coronary heart disease, autopsy revealed a bolus of food, often steak, lodged in the pharynx
or larynx. In any choking on food, the bolus can be quite large, such as a whole pancake, a whole tangerine, or masses of meat, fruit, or vegetable. Senile
persons in retirement homes, and mentally retarded children in institutions are also vulnerable. In such fatalities, the history and mode of death gives no
hint of a hypoxic mechanism. Many cases have been observed in which the victim merely sits back in their chair, dead -- the mode clearly being cardiac
arrest, presumably from overactivity of the parasympathetic nervous system from stimulation of the laryngeal or pharyngeal mucosa -- the so-called "vasovagal
reflex" or "reflex cardiac inhibition."
From chapter 15: "Fatal Pressure On The Neck"
Overview (page 368)
"This provides one of the most complex and controversial areas of 'asphyxial' deaths, as the mechanism is uncertain and the frequency of such deaths makes
them a common problem for both forensic pathologist and jurist...Strangulation was formerly thought to be a pure asphyxia as a result of "cutting of the
air" by occlusion of the airway during the constriction of the neck. Since the end of the 19th century, however, it has been recognized that the rapidity
of death in many cases made it impossible for hypoxia to the the sole or even a major cause. Many victims died almost immediately and exhibited none of
the so-called "classic signs" of asphyxia. Others, though showing these signs, still died too quickly for it to be reasonably argued that lack of oxygen
had proceeded to a fatal stage.
Picture caption (page 369)
Figure 15.2. Possible effects of pressure on the neck: (A) carotid sinus reflex leading to cardiac arrest; (B) jugular venous distention leading to
cyanosis and petechiae; (C) carotid artery compression leading to unconsciousness; and (D) airway obstruction leading to hypoxia.
Nerve effects (page 369)
Pressure on the baroreceptors situated in the carotid sinuses, the carotid sheaths, or the carotid body, can result in bradycardia (slowing of the heart)
or in total cardiac arrest...It is often claimed, admittedly without much concrete evidence, that fear, apprehension, struggling, and possibly the effect
of drugs such as alcohol, may heighten the sensitivity of this vagal mechanism. The release of catecholamines during such adrenal responses may well
sensitize the myocardium to such neurogenic stimulation.
Nerve effects (continuing on page 370)
The vagal reflex has profound implications in relation to pressure or blows on the neck. Sometimes called "vagal inhibition," "vagal shock," or "reflex
cardiac arrest," the rapid onset of heart stoppage may antedate any evidence of congestive or "asphyxial" signs, causing death immediately, or within
seconds, or at anytime thereafter.
It is a matter of some dispute as to whether this reflex can cause immediate cardiac arrest or whether there has to be a period of marked slowing of the
heart with negligible cardiac output -- or whether an arrhythmia such as ventricular fibrillation precedes such an arrest. Probably any combination can
occur, but it is an indisputable fact that collapse and apparent death can occur immediately on application of pressure to the neck. Overstimulation of
nerve endings in the carotid sinus or adjacent arterial sheath may be brought about by direct pressure from fingers, or from a ligature from strangulation
or hanging -- or from a blow directed at the side of the neck. Severe pain, such as a blow to the larynx or genitals, may also trigger a vagal response.
THE FREQUENCY OF VAGAL CARDIAC ARREST
Though different authors vary in the proportion of such deaths that they attribute to reflex cardiac arrest, they all admit to the existence of such a
mechanism. In the author's (BK) own series of fatal pressure on the neck from a variety of causes, the "classical signs," denoting vascular and sometimes
airway obstruction, were present in slightly less than half the cases. The remaining deaths presented with an absence of congestion, cyanosis and
petechiae, the pale faces indicating that cardiac arrest had taken place before the congestive signs had time to appear.
MEDICO-LEGAL ASPECTS
This phenomenon has considerable legal as well as medical significance, as sudden death from "vagal inhibition" can occur with total unexpectedness even
with relatively light pressure to the neck. Keith Simpson and Polson reported cases many years ago in which a soldier at a dance playfully "tweaked" his
partner's neck and was mortified to see her drop lifeless to the floor. Many such cases are on record and every forensic pathologist of any experience has
examples in his own records. Where it can be shown that the death occurred rapidly and without prolonged gripping of the neck, the defense may be raised
that neither death nor serious injury was intended by the accused. If would be much harder to establish this lack of intent if the grip was maintained long
enough to lead to florid congestion and petechiae of the face.
A COMBINED MECHANISM OF INJURY AND DURATION OF NECK COMPRESSION
It is important to remember that the cardiac arrest mode of death may be mixed with the congestive-petechial mode in that, though the first stages of
pressure may continue for long enough for congestive-asphyxial signs to appear (perhaps a minimum of 15-30 seconds), a change in grip may then allow the
fingers to impinge on the carotid structures and lead to reflex cardiac arrest. Thus the progression of the pure "asphyxial" process may be abruptly
terminated at any point along its pathway to death by the superimposition of "vagal inhibition," so the intensity of congestive changes may be of any degree
in any given death.
(Continuing on page 371)
The duration for which pressure must be maintained is often a contentious issue during criminal trials, as the "inadvertent squeeze" that causes rapid vagal
cardiac arrest is likely to be viewed as less culpable than a prolonged, unremitting gripping of the throat.
It is virtually impossible to measure the average minimum time of gripping that will produce congestion, cyanosis, and petechiae from venous occlusion. As
so often is the case in forensic medicine, animal experiments are useless for this purpose and obviously few cases of strangulation homicide are reliably
witnessed, especially by some dispassionate observer with a stopwatch!
CAUSES OF REFLEX CARDIAC ARREST
Vagal inhibition of the heart from stimulation of the carotid neural complex may occur in any form of pressure on the neck, but is much more common with
manual strangulation than with a ligature, hanging excepted. Fingers seem more prone to dig deeply and find the structures under the anterior edge of the
sternomastoid muscle. Perhaps the movement of the fingers, especially during the shifting postures of a struggle, more readily impinge upon the carotid
bifurcation than the more static position of a ligature.
The majority of hangings, however, present with a pale face, free from congestive -haemorrhagic signs. This seems to be caused by the more precipitate
impact of the noose on the carotid structures when the victim's weight abruptly bears down, though Polson favored actual carotid occlusion and hence carotid
ischemia as the common cause of death in hanging. The scarcity of carotid intimal damage in suicidal hangings does not favor this view.
BLOWS TO THE THROAT
Another cause for sudden cardiac arrest is a blow to the neck or throat. This is the basis of the so-called "commando punch" and some of the oriental martial
arts also contain this in their repertoire -- often forbidden because of its potential lethality. The edge of the hand is brought forcibly across the side of
the neck or the front of the larynx.
Direct violence to the carotid region naturally causes gross stimulation of the afferent nerve endings. Blows directly to the larynx indirectly stimulate the
sinus region or the laryngeal sensory nerve endings may themselves trigger the cardio-inhibitory reflex.
It is well known that the hypopharynx and larynx are particularly sensitive to stimulation, which accounts for the sudden deaths from impaction of food in
the larynx, or from the flooding with cold water that causes some sudden immersion deaths. The testicles and uterine cervix also have a similar reputation
for leading to sudden cardiac death, if unexpectedly stimulated, especially when the myocardium is pre-sensitized by catecholamines released by fear or emotion.
DAMAGE TO THE CAROTID ARTERIES (Page 378)
Though the sudden "vagal inhibition" type of death caused by pressure on the baroreceptors of the carotid sinus and sheath is quite common, it is unusual to
find anatomic confirmation of injury to these structures.
(Continuing on page 379)
As already mentioned, one problem is that the pressure may be maintained for long enough -- perhaps a minimum of 15 to 30 seconds -- to produce these signs, yet
not cause death, but death then supervenes abruptly because a vagus-mediated cardiac arrest is superimposed on the early asphyxial mode.
STRANGULATION BY LIGATURE
(Page 381)
Figure 15.20: Self-strangulation by ligature, with three turns around the neck and a complex knot. There was no doubt from the circumstances that the deceased
man had deliberately killed himself with this telephone cord, but the mechanism of apparent vasovagal death before any congestive changes could appear remains
obscure.
(Also from Page 381)
[Here, the author is talking about post-death swelling of the tissues.] In suicides, multiple turns and knots may have been applied and, obviously the degree
of tightness as seen later at autopsy could not have been present during the application of the ligature, otherwise incapacity would have been so rapid that
the process could not have been completed. In such cases, it is remarkable how often the mode of death still seems to be of the non-asphyxial cardiac arrest
type. It might be suspected that vagal stimulation could not have occurred once the expected static position was obtained with the completion of
ligation -- but experience indicates otherwise, the mechanism remaining obscure.
THE MODE OF DEATH IN LIGATURE STRANGULATION (Page 382)
The mode of death is more often of the "classic asphyxia" picture than in manual strangulation, where sudden cardiac death is common before congestive-petechial
changes have time to occur...This is by no means invariable, and many ligature strangulations die rapidly from vagal reflex cardiac arrest before congestive
signs have time to appear.
ARM-LOCKS AND "MUGGING" (Page 383)
The original meaning of "mugging" has now been confused by its application, especially in North America, to any form of robbery with violence. The
term strictly means throttling by pressure from an arm held around the throat. The attack is usually made from behind, the neck being trapped in the crook of
the elbow. Pressure is then exerted on either the front of the larynx, or at one or both sides by the forearm and upper arm. The mechanism is further discussed
in Chapter 10 as an arm-lock (or "choke-hold") is a method of restraint used by police officers for law enforcement, but it is rapidly losing favor because of
the number of inadvertent fatalities due either to "asphyxia" or reflex cardiac arrest. Following several fatalities during police arrests in the early 1990s,
the association of Chief Police Officers in Britain have issued recommendations that arm-locks be avoided during the restraint of violent prisoners.
SUICIDAL AND ACCIDENTAL HANGING (Page 384)
Hanging has many features in common with ligature strangulation. Death is, however, more often caused by reflex cardiac arrest from pressure on the carotid
structures. Many more victims of hanging are found to have pale faces, rather than the congested, hemorrhagic appearance of the slower asphyxial type of death.
Page 385
Figure 15.25: Suicidal hanging by means of a necktie. The deceased man had suspended his neck from a hook on the back of a door by tying two neckties
together. The hook had pulled out and he was found on the floor. Note the pale, uncongested face, indicating a rapid cardiac death.
Page 388
Figure 15.34: Suicidal hanging with the rope in a frontal position. Even though the larynx cannot be compressed, death is due to pressure on the carotid
arteries and sinuses. The face is pale, with no so-called "asphyxial signs."
MECHANISM OF HANGING
There are a number of mechanisms by which hanging may cause death, which may act independently or in concert. These include: stretching of the carotid sinus
causing reflex cardiac arrest; occlusion of the carotid (and possibly vertebral) arteries; venous occlusion; airway obstruction resulting from pushing the
base of the tongue against the roof of the pharynx or from crushing of the larynx or trachea; and finally spinal cord-brainstem disruption.
While hanging shares some features with manual strangulation, the majority of victims of hanging are seen with pale faces, rather than the congested, hemorrhagic
appearance associated with the slower death associated with pressure on the neck. This probably reflects a different mechanism, with reflex cardiac arrest and
carotid occlusion more prevalent in hanging than in strangulation. Such mechanisms cause death rapidly, with unconsciousness resulting from bilateral occlusion
3-11 seconds after application of the circumferential pressure.
However the precise interplay of different mechanisms, which themselves appear only partially dependent on the completion of suspension and the location of the
noose, is impossible to determine from the pathological findings alone.
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