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This term refers to all forms of syncope that result directly from the vascular effects of neural signals coming from the CNS, primarily the nucleus tractus solitarius (NTS) A number of stimuli, mostly from the viscera but some of psychologic origin, are capable of eliciting this response, which consists of a reduction or loss of sympathetic vascular tone coupled with a heightened vagal activity The NTS in the medulla integrates these afferent stimuli and normal baroreceptor signals with the efferent sympathetic mechanisms that maintain vascular tone (see further on and Chap 26) Several lines of study suggest that there are disturbances of both sympathetic control of vascular tone and also of the responsiveness of baroreceptors By the use of microneurography, Wallin and Sundlof have demonstrated an increase in sympathetic out ow in peripheral nerves just prior to syncope as would be expected; this activity then ceases at the onset of fainting Unmyelinated (postganglionic sympathetic) bers cease ring during vasovagal fainting at a point when the blood pressure falls below 80/40 mmHg and the pulse below 60 This would signify that there is an initial attempt to compensate for the falling blood pressure, following which there is a centrally mediated withdrawal of sympathetic activity Which one of these mechanisms (perhaps both) is responsible is not clear More recently, Bechir has shown that muscle sympathetic activity as assessed using microneurography is increased in the resting state in patients with orthostatic hypotension and, importantly, does not increase further with venous pooling (induced by lower-body negative pressure) Moreover, in the same patients, the response of the cardiac baroreceptors to pooling was signi cantly diminished These data are partially in agreement with those of Wallin and Sundlof, although they are not in accord with an initial increase in sympathetic activity prior to syncope The clear implication of such studies is that the ability of the sympathetic nervous system to compensate for falling blood pressure is impaired, although it is not clear whether the primary defect is at the level of the baroreceptor afferents, the nucleus solitarius, or the sympathetic effector neurons There is agreement that peripheral vascular resistance is greatly reduced just prior to and at the onset of fainting This drop in resistance has been attributed by some to an initial adrenergic discharge that, at high levels, causes a vasodilation (rather than constriction) in intramuscular blood vessels High levels of epinephrine and the vasodilating effects of nitric oxide acting on vascular endothelium as well as greatly augmented levels of circulating acetylcholine during syncope have also been invoked as additional or intermediary factors, but all remain speculative In the current view, the drop in blood pressure is the result of a transient but excessive activity of sympathetic nerves that paradoxically leads to vascular dilatation in muscle and viscera It has been further suggested, on the basis of reasonable but not conclusive physiologic evidence, that the early sympathotonic attempt to maintain blood pressure leads to overly vigorous con-.

The commands option within the WAD is not really a Web item, nor is it something that is available on its own It s an additional component of a number of different Web items During the configuration of a particular Web item, such as a Button Group, you would use a command There are many different commands for both the Web reports and the planning process There are over 50 of these commands and they are closely connected, but we will focus on just the Web-related commands to see what they can do for us in terms of improving the dashboard s functionality and final results In the WAD, the command wizard is the main tool for creating commands from the Web Design API You can use it to create commands easily by following a step-by-step procedure and include them in your Web template, enabling you to create highly individual Web applications with BI content There are a number of approaches to making a command available in the Web template and dashboard that you are creating: Use the normal button format available Create a hypertext link to execute a command process Set up the command to be executed via a context menu

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and Zoterman and came to be known as the Bezold-Jarisch re ex The inferoposterior wall of the left ventricle is the site of most of the subendocardial mechanoreceptors that are responsible for the afferent impulses In order for this mechanism to become active, very vigorous cardiac contractions must occur in the presence of de cient lling of the cardiac chambers (hence neurocardiogenic ) In the simple faint, an initial burst of sympathetic activity is thought to precipitate these physiologic circumstances of excessive cardiac activity Echocardiographic ndings of a greatly diminished ventricular chamber size and vigorous contractions just prior to syncope support this notion (the empty-heart syndrome ) However, the ability to induce a similar neurally mediated syncope in cardiac transplantation patients, whose hearts are denervated, leads one to question this concept Perhaps the remaining baroreceptors in the aorta are responsible in this instance According to Kaufmann, a proclivity to primary neurocardiogenic syncope can be identi ed by the nding of delayed fainting when the patient is placed at a 60-degree upright position on a tilt table After approximately 10 min of upright posture, the blood pressure drops below 100 mmHg; soon thereafter, the patient complains of dizziness and sweating and subsequently faints In contrast, patients with primary sympathetic failure will faint soon after upward tilting Half of patients with unexplained syncope display this delayed tilt-table reaction, but it is also seen in 5 percent of controls (see pages 330 and 459) The value of isoproterenol as a cardiac stimulant and peripheral vasodilator to enhance the effect of upright posture and expose neurocardiogenic syncope during the tilt-table test is controversial, as described further on, under Special Methods of Examination Exercise-Induced Syncope Aerobic exercise, particularly running, is known to induce fainting in some persons, a trait that may become apparent in late childhood or later and may be familial There is nausea as well as other presyncopal symptoms; the faint can be avoided by discontinuing exercise or not exceeding a threshold of effort set by the patient himself Such persons do not seem unduly sensitive to nonaerobic exercise and have no recognizable electrocardiographic or structural heart problems They have a predilection to faint with prolonged tilt-table testing and with isoproterenol infusion, suggesting that this represents a form of neurocardiogenic syncope For this reason, these patients may bene t from beta-adrenergic blocking drugs if given under careful supervision As discussed further on, exercise can also precipitate syncope in patients with a number of underlying cardiac conditions (myocardial ischemia, long QT syndrome, aortic out ow obstruction, cardiomyopathy, structural chamber anomalies, exerciseinduced ventricular tachycardia, and less often supraventricular tachycardias) Athletes who faint unpredictably during exercise pose a particularly dif cult problem Obviously those found to have serious heart disease should give up competitive sports, but the majority have no demonstrable cardiac abnormality Subjecting these patients to intense exercise and other testing sometimes fails to elicit the faints, but many have varying degrees of hypotension when subjected to prolonged head-up tilt, again suggesting that the cause of fainting is essentially neurocardiogenic (see above) Standard pacemakers are not curative in these vasodepressor faints, since the main de ciency is in vascular resistance Unless the results of tilttable testing are unequivocal and reproducible, it is best to consider.

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