I had no intentions of throwing a bouncer. What I wanted to emphasize was that more often than not, baroreceptors are not involved in cases of NMS. They may be involved in a few (not that they lead to NMS but their dysfunction might be involved in failure to counter the fall in BP and bradycardia, be it orthostatically induced, or centrally mediated. This dysfunction is more likely to occur at central sites of the reflex loop rather than at the receptor level or in the effector organ - barring a few instances like diabetic peripheral autonomic neurodegenerative disease). Earlier theories (like those of Sharpey Schaffer) also did not hold arterial and cardio-pulmonary baroreceptors responsible for NMS but a Bezold-Jarisch type of phenomenon due to left ventricular mechanoreceptor activation. There are few takers for these theories today. As I cannot indefinitely prolong this e-mail, I am attaching two relevant pdf files on the subject for the benefit of all. Hope these will clarify the situation a little bit. Sudhanshu ----- Original Message ----- From: "USM Bish" <bish@xxxxxxxxxxx> To: <indaemed@xxxxxxxxxxxxx> Sent: Monday, March 22, 2004 12:19 AM Subject: [Indaemed_Freelist.Org] Vaso-Vagal-Syncope [was Syncope evaluation [was Re: Re: NMS]] > On Sun, Mar 21, 2004 at 01:39:22PM +0530, SS Mishra wrote: > > > > First of all, VVS is not essentially a baroreceptor induced > > phenomenon !!!!!!! > > > > I am not certain what the latest journals say on the subject, > but as I understand VVS is not a primary entitly, it is merely > a response phenomenon (which has neuro-vascular components). > > > Today, more and more evidence is gathering for it to be a > > centrally mediated process. > > It was no different when I did my I MBBS over 30 years ago ! > The live example of VVS (explained by our Prof) was the > fainting spell one girl in our batch had on the sight of blood > being drawn from her veins ! Surely, the origin was central > (psychological), but the manifestation was through ANS/ > baro-receptor based physiology. He explained the whole process, > and I remember it clean as being baro-receptor mediated. Things > may have changed now, but frankly, I am quite unaware of these > recent changes in the explanation process. > > I tried to find out over the internet, but could not find any- > thing in this regard. To the contrary, a search for vaso vagal > syncope on google threw out 957 links. One of the first was > from the Univ of Columbia, Neurology Dept. This is aimed at lay > audience (Patient information, as they call it). > > This are the first three paras: > > ------------------------<snip>--------------------------------- > > What is vaso-vagal syncope? > > Vaso-vagal syncope is the medical term for a common cause of > fainting. In this disorder, the nervous reflexes which control > heart rate and blood pressure behave abnormally causing a drop > in blood pressure and a fainting spell. > > The nerves which control the heart rate and blood pressure are > regulated through pressure sensors in the arteries and veins > called the baroreceptors. The baroreceptors detect changes in > blood pressure. These baroreceptors detect a fall in blood > pressure and send signals via the nerves to increase the heart > rate and constrict blood vessels bringing the blood pressure > back to normal. Conversely, baroreceptors detect abnormally > elevated blood pressure and send signals to slow heart rate and > relax blood vessels to lower blood pressure back to normal. > These reflexes are called the baroreflexes. > > Vaso-vagal syncope results from an abnormality in the > baroreflexes. When you stand up, the force of gravity causes > some of the blood from your heart and your chest cavity to pool > in your legs. This produces a slight drop in blood pressure > which is detected by the baroreceptors and is adjusted through > the baroreflexes. In patients with vaso-vagal syncope, after a > period of standing in the upright position, baroreflex > adjustments fail and blood pressure and heart rate decrease > causing fainting. > > [ Rest snipped ... goes to other examples and tilt table ] > > -------------------------</snip>------------------------------- > > > And this is from heartdisease.about.com: > > ------------------------<snip>--------------------------------- > > [ First portion pertaining to vasomotor syncope excluded] > > Vasovagal syncope (also known as cardioneurogenic syncope) is > the most common cause of syncope, probably accounting for more > than 80% of all syncopal episodes. Since vasovagal syncope is > simply an exaggeration of a normal neurological reflex, most > individuals will experience at least one vasovagal episode in > their lifetimes. > > The reflex responsible for vasovagal syncope works like this: A > person is exposed to some stimulus (such as a needle stick) > that initiates the reflex. The "stimulated" nerves (the nerves > of the stuck finger, for instance) send an electrical signal to > the vasomotor center in the brainstem. (The vasomotor center > determines the body's vascular "tone.") The vasomotor center, > in turn, signals the blood vessels in the legs to dilate, > causing the blood to pool in the legs, and producing syncope. > This same reflex also causes a drop in the heart rate, but > usually it is the pooling of blood in the legs - and not the > slow heart rate - that produces loss of consciousness. > > The "stimulus" that triggers a vasovagal episode can be any one > of hundreds of things. As already noted, pain is a common cause > of fainting. Other common triggering events include the sight > of blood, receiving upsetting news, or standing motionless for > long periods (such as with soldiers standing at parade rest). > > Anyone can have vasovagal syncope given an adequate triggering > event, but many people are particularly prone to these > episodes, and often with relatively mild triggers. These > individuals tend to relate histories of syncope dating back to > adolescence, and frequently will describe several different of > triggering events. While, as noted, there are scores of > possible triggering events for vasovagal syncope, some are > quite characteristic and almost always point to vasovagal > syncope. Syncope occurring after urinating, defecating, > coughing or swallowing, or syncope associated with pain, > fright, the sight of blood, or other noxious stimuli, is almost > always vasovagal. > > In these and other ways, vasovagal syncope tends to be highly > situational. It is more likely to occur after a viral illness, > after exercise, after a warm shower, or early in the morning - > any time that relative dehydration is present, and dilation of > the blood vessels in the legs would be more likely to produce a > significant drop in blood pressure. Furthermore, vasovagal > syncope is often preceded by a few seconds or a few minutes of > warning symptoms. Often, these symptoms include > lightheadedness, ringing in the ears, visual disturbances, > sweating and/or nausea. Because of such "warning symptoms," > people who have had one or two episodes of syncope are > frequently able to tell when an event is about to occur. And > importantly, if they recognize the warning symptoms, they are > able to abort the blackout simply by lying down and elevating > the legs. ("Aborting" syncope is not possible with most other > forms of syncope.) > > Given these characteristic features and the situational nature > of this condition, doctors can make the correct diagnosis in > the vast majority of patients with vasovagal syncope simply by > asking right questions and listening carefully to the answers. > > ------------------------</snip>-------------------------------- > > The fact remains, that my understanding on the subject, is > perhaps more detailed than what is stated above, but definitely > in line with these. If things have changed drastically from the > above, it is time to re-educate ourselves. Could we have the > references (if readily available), or anything on the net ? Or > could you post a "recent thinking" type of discourse on this > list ? > > Ready to receive the next Shoib delivery .... > > Bish > > >