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« on: October 17, 2012, 02:18:23 PM »

A Complete Health E-Guide

Vagal inhibition
May 31, 2012 | Filed under: Forensic Medicine,General Health | Posted by: admin

Vagal inhibition is condition that causes sudden death to occur within seconds or a minute or two due to minor trauma or relatively simple and harmless peripheral stimulation.
Pressure on the baroreceptors situated in the carotid sinuses, carotid sheaths, and the carotid body (located in the internal carotid artery just above the bifurcation of common carotid artery, and situated about the level of angle of mandible) causes an increase in blood pressure in these sinuses with resultant slowing of the heart rate, dilatation of blood vessels and a fall in blood pressure. The vagal inhibition leaves the person dead instantly.
In normal persons, pressure on the carotid sinus causes minimal effects with a decrease in heart rate of less than six beats per minute, and only a slight reduction (less than 10 mm. Hg) in blood pressure. Some individuals show marked hypersensitivity to stimulation of the carotid sinuses, characterized by bradycardia and cardiac arrhythmia ranging from ventricular arrhythmias to cardiac arrest.

vagal inhibition

Stimulation of the corotid sinus baroreceptors causes impulses to pass via Herring nerve to the afferent fibers of the glossopharyngeal nerve (9th cranial nerve) ; these in turn link in the brain stem to the nucleus of the vagus nerve (10th cranial nerve) causing the vagal inhibition.
Parasympathetic efferent impulses then pass to the heart via the cardiac branches of the vagus nerve. Stimulation of these fibers causes a profound bradycardia. This reflex arc is independent of the main motor and sensory nerve pathways. There is wide network of sensory nerves in the skin, pharynx, glottis, pleura, pentoneum covering viscerr or extending into the spermatic cord, cervix, urethra, perineum and coeliac plexus.
Afferent fibers from these tissues pass into the lateral tracts of the spinal cord, effect local reflex connections over several segments and also pass to the brain. The vagal nucleus is controlled by the synaptic connections in the spinal cord, which may be facilitated from both the sensory central cortex and from the thalamic centres. The latter may be responsible for emotional tone noted in the vagal reflex.
Parasympathetic stimulation of the heart can be initiated by high neck compression, pressure on carotid sinus or sometimes by direct pressure over the trunk of the vagus nerve.
Causes of vagal inhibition
(1) The commonest cause of such vagal inhibition is pressure on the neck particularly on the carotid sinuses as in hanging or strangulation.
(2) Unexpected blows to the larynx, chest, abdomen and genital organs.
(3) Extensive injuries to the spine or other parts of the body.
(4) Impaction of food in larynx or unexpected inhalation of fluid into the upper respiratory tract.
(5) Sudden immersion of body in cold water.
(6) The insertion of an instrument into the bronchus, uterus, bladder or rectum.
(7) Puncture of a pleural cavity usually for producing a pneumothorax.
(8 ) Sudden evacuation of pathological fluids, e.g., ascitic or pleural.
(9) Sudden distension of hollow muscular organs, e.g., during attempts at criminal abortion, when instruments are passed through the cervix or fluids are injected into the uterus.
(10) In degenerative diseases of the heart, e.g., sinus bradycardia and partial or complete A-V block; parasympathetic stimulation further depress the heart rate and may induce a Stokes-Adams attack which may be fatal. There is great variation in individual susceptibility.
Death from vagal inhibition is accidental and caused by microtrauma. The stimulus should be sudden and abnormal for the reflex to occur. The reflex is exaggerated by a high state of emotional tension, and also any condition which lowers voluntary cerebral control of reflex responses, such as a mild alcoholic intoxication, a degree of hypoxia or partial narcosis due to incomplete anesthesia.
When death results from vagal inhibition, there are no characteristic postmortem appearances. The cause of death can be inferred only by exclusion of other pathological conditions, and from the accurate observations by reliable witnesses, concerning the circumstance of death.

A soldier was dancing with his girl friend in the presence of many others in a hall. While dancing, he playfully ‘tweaked” (pinched) her neck. She dropped down dead on the spot. There were no injuries or signs of asphyxia. Death was as a result of vagal inhibition.


Director of the Conjoint Laboratories of the Royal Colleges of Physicians and Surgeons, London, AND A. E. RUSSELL, M.D., Resident Assistant Physician, St Thomas's Hospital, London. (Six Figures in Text.)

(From the Conjoint Laboratories of the Royal Colleges of Physicians and Surgeons, London.)

IT has long been known that slowing or arrest of the heart can be brought about reflexly by excitation of almost any afferent nerve of the body if the stimulus be sufficiently great, and that the one nerve which can most readily produce this reflex effect is the vagus. The systematic examination of the different branches of the vagus with the direct object in view of determining which fibres play the most important part in producing the reflex has not however been carried out. Hence the experiments described in this paper have been designed.

Our experiments can be conveniently grouped for descriptive purposes in two sections, in the first of which we deal with the results obtained by electrical excitation of the vagal branches and in the second, with other modes of excitation,-chemical, mechanical, etc. -which followed as a direct consequience of the results we obtained in our first series.

Most of our experiments have been performed upon dogs, the anaesthetic employed being, as a rule, the A.C.E. mixture. In a few cases urethane was used, which was administered either subcutaneously or by intravenous injection; the dose given was 1-25 grm. per kilo of body weight. The results were precisely the same with both forms of anaesthesia. We have also confirmed our results upon cats and found the reaction the same in this animal as in the dog.

To record the effect upon the heart we usually took the carotid blood-pressure curve as being on the whole the most convenient. The records thus obtained were always checked by direct observation of the heart in those experiments in which it was exposed, by palpation, or by placing a finger upon an artery while the nerve stimulation was being carried on. We also tested whether the effects were exerted upon all four cavities of the heart uniformly, by recording the conttactions of the ventricles and auricles. We found that whenever any slowing of the heart took place it was to be observed equally in both ventricles, and in auricle as well as ventricle.

Brodie, T. G., Russell, A. E., (1900), On reflex cardiac inhibition. The Journal of Physiology, 26 doi: 10.1113/jphysiol.1900.sp000824.

I was nearly killed by that thing. My story made it to Reader's Digest.,4490.0.html

« Last Edit: September 06, 2016, 03:40:49 AM by dennis100 » Logged
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« Reply #1 on: June 04, 2014, 01:08:34 PM »

Regulation of Ventricular Contraction Influence of Cardiac Sympathetic and Vagal Nerve Stimulation on Atrial and Ventricular Dynamics

At constant heart rates, efferent stimulation of the vagus nerve and of the left stellate ganglion revealed the following:

1. Vagal stimulation exerts a profound depressant effect on the strength of the atrial contraction and can thereby influence ventricular filling and ventricular stroke work; it elevates mean atrial pressure at any given level of ventricular stroke work. This occurs under experimental conditions wherein the vagal stimulation used does not produce an alteration in the performance characteristics of the ventricle. The effects of vagal stimulation are blocked by atropine.

2. Stellate ganglion stimulation or norepinephrine infusion augments the strength of atrial contraction and thus the atrial contribution to ventricular filling. The augmented atrial contraction takes place in a shorter period of time.

3. Stellate ganglion stimulation or norepinephrine infusion increases the external stroke work and power produced by the ventricle from any given mean atrial pressure and from any given end-diastolic pressure or fiber length.

4. There is a family of curves representing the relation between end-diastolic fiber length and stroke work, as well as a family of curves representing the relation between mean atrial or end-diastolic pressure and stroke work.

5. When taken together with the well-known sympathetic and parasympathetic effects on heart rate, the above data are believed to comprise a reasonably comprehensive description of the means available to the central nervous system for directly inducing acute changes in the activity of the heart.
« Last Edit: September 06, 2016, 01:34:12 AM by dennis100 » Logged
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« Reply #2 on: June 30, 2014, 02:33:26 AM »

Nervus vagus belongs to parasympathetic nervous system which inhibits the contraction of heart, decreases its excitability and frequency of generated nerve impulses in heart. By overstimulating n.vagus these effects on heart are more intense - it could lead to total inhibiton of heart contractions, which would eventually lead to death within a little while.

Very intense slap behind ear or intensive pressure on neck area could lead to death as n.vagus is overstimulated. It is very rare though.
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« Reply #3 on: June 30, 2014, 08:21:52 AM »

Future indicators for VNS therapy:

Alcohol addiction

Alzheimer's Disease


Atrial fibrillation



Bulimia Nervosa

Burn-induced organ dysfunction

Chronic heart failure


Dramatic first words spoken in 2 children after vagus nerve stimulation

Dravet syndrome



Gut injury and lung permeability in trauma-hemorrhagic shock



Inhibits heroin-seeking behavior in rats

Intestinal epithelial barrier breakdown

Lennox-Gastaut syndrome

Medication-refractory mental illness


Migraine and Cluster Headaches

Mood disorders in elderly population

Multiple sclerosis



Positive effect on mood in patients with refractory epilepsy

Peripheral arterial occlusion disease

Postoperative cognitive dysfunction in elderly patients

Posttraumatic epilepsy

Reduces infarct size

Ringing in the ears


Severe anxiety disorders

Severe mental diseases

Spinal trigeminal neuronal

SUDEP in children and adolescents


Tourette's Syndrome

Transient focal cerebral ischemia

Trauma-hemorrhagic shock

Traumatic brain injury

Visceral pain-related affective memory

This one is in the trial phase:
Vagus Nerve Stimulation to Augment Recovery From Minimally Conscious or Persistently Vegetative States After Traumatic Brain Injury

« Last Edit: September 06, 2016, 11:28:35 AM by dennis100 » Logged
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« Reply #4 on: June 30, 2014, 09:21:31 AM »

Model Number 105
Event Date 04/28/2014
Event Type Injury
Event Description
It was reported that during the patient's initial implant surgery on (b)(6) 2014, there were difficulties identifying the nerve due to a structure with a similar appearance. Therefore, following placement of the electrodes on the structure believed to be the vagus nerve, the patient¿s generator was programmed on (output current - 2ma) in an attempt to induce bradycardia and therefore identify if the electrodes were indeed on the vagus nerve. Bradycardia was observed as intended and resolved without intervention. Therefore, it was concluded that the electrodes were properly placed. The generator was inadvertently not programmed off after the tests were completed due to communication difficulties with the programming system. As a result, the patient experienced painful stimulation, neck muscle spasms, and severe coughing until the surgeon programmed the patient's generator off and administered morphine the following day.

Model Number 102
Event Type Injury
Event Description
Attempts for additional information have been unsuccessful to date.
Manufacturer Narrative

Event Description
A cardiac electrophysiologist called to inquire about precautions for placing a pacemaker in a vns patient. It was reported that the patient's neurologist suggested she get a pacemaker due to asystole; however, caller was unsure of the relationship of this to their vns. Good faith attempts are underway for further details about the reported event.

Event Date 01/07/2011
Event Type Injury
Patient Outcome Life Threatening; Required Intervention
Event Description
It was reported that the pt went to the clinic to have the vns turned on. The pt was programmed to 0. 25 ma and could feel stimulation. When the nurse left the room for a few minutes, the pt's parent alerted that the pt had collapsed on the floor, was non-responsive and chalky white. The nurse thought this may have been due to the vns and turned the device off. The pt was resuscitated and transferred to intensive care unit and now reported to be recovering. The pt's heart rate after device switched off and during resuscitation was 60 bpm. There are no further plans to date.

Model Number 103
Event Date 08/23/2013
Event Type Injury
Manufacturer Narrative

Event Description
It was reported that the vns patient has been in the hospital icu with bradycardia and has coded at least once. A company representative went to the hospital to perform device diagnostics which were reported to be within normal limits. It was reported that the patient underwent cardiac workup and that the cardiologist found only vns as a potential source of the bradycardia. It was reported that the arrythmia events are not occurring with stimulation and they occur infrequently; however, the patient has had to be revived once or twice. The neurologist decreased the output current from 2. 5ma to 1. 5ma and is going to evaluate the patient to see if that helps. It was reported that there were no setting changes or medication changes that preceded the onset of the bradycardia. The patient's mother reported that the patient did not have any prior history of cardiac events.

Event Description
Additional information was received from the neurologist stating that the patient¿s bradycardia was possibly related to vns. The patient¿s device was programmed off. The patient did not have a medical history of bradycardia prior to vns.

Manufacturer Narrative
Date of event, corrected data: the initial manufacturer report incorrectly reported the date of the event.

Model Number 102
Event Date 01/01/2006
Event Type Injury
Event Description
Vns pt was hospitalized with asystole. While hospitalized, the pt's device was programmed to off, after which his condition stabilized. While attempting to reinitiate device stimulation, the pt exhibited asystole again. Treating physician programmed the device back to off and does not plan to reinitiate stimulation. The pt had reportedly been experiencing good seizure control with the vns therapy and his device had been programmed to 3. 0ma normal mode output current "for quite a while". It was reported that since the incident, the pt is unable to tolerate even lower levels of stimulation, due to the cardiac condition. The pt is non-verbal and cannot communicate whether device stimulation feels abnormal. The pt does not have any pre-existing conditions that may have precipitated the reported event and there had been no recent changes to the pt's medication regimen.

more reports
« Last Edit: September 06, 2016, 04:51:46 AM by dennis100 » Logged
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