What is Neurocardiogenic Syncope?
Neurocardiogenic syncope is a temporary loss of consciousness associated with a drop in arterial blood pressure, quickly followed by a slowed heart rate (Grubb & McMann, 2001, p. 133).
Neurocardiogenic syncope (NCS) is also referred to as vasovagal syncope or neurally mediated syncope. The terms are used interchangeably throughout this web page.
What are the symptoms of NCS?
Neurocardiogenic fainting usually occurs while standing. Emotional stress, stressful condition and pain may trigger an episode, especially among the young (Shah, Gupta & Lokhandwala, 2003). The onset may be abrupt or associated with warning symptoms such as fatigue, weakness, nausea, sweating, pallor, visual disturbances, abdominal discomfort, headache, pins-and-needles, lightheadedness or vertigo (Deering, 2003). Presyncopal patients may also complain of palpitations, vomiting, disorientation, and difficulty speaking clearly or coherently (Grubb & McMann, 2001, p. 60.). Other symptoms that may present before a faint include feeling either warm or cold, tremors, yawning and having a bluish/purple or red coloring to the skin (Alboni, Brignole, Menozzi, Raviele, Del Rosso, Dinelli, Solano & Bottoni, 2001).
During the faint "seizure-like" activity may occur (Grubb, Gerard & Roush, 1991). This convulsive activity is thought to be distinct from a seizure disorder.
Patients are sometimes symptomatic after a faint as well. Patients may complain of symptoms including nausea, clamminess, lightheadedness, headache and malaise (Deering, 2003). Patients may also experience vomiting, abdominal discomfort, weakness, tremors, cold or warm feelings and confusion (Alboni et al., 2001). Patients who experience frequent neurocardiogenic syncope may report symptoms between faints as well, such as chronic fatigue, headache, chest pain, exercise intolerance, heart "flip flops" and an inability to tolerate prolonged standing.
Mechanisms and Causes of NCS
When a person stands up, the pull of gravity causes blood to pool in the lower extremities. This can result in a lack of blood supply to the upper body, including the heart and brain. Normally, the body automatically adjusts to the lack of blood supply by increasing vascular tone, heart rate and cardiac output. Blood vessels contract, heart rate increases, systolic blood pressure remains about the same or drops slightly while diastolic pressure rises slightly (Brunner & Suddarth, 2000, p. 546).
In those with neurocardiogenic syncope this compensatory mechanism does not always work correctly. The exact mechanisms of NCS are not completely understood, and several theories have been proposed. Many physicians hold a general consensus as to what is happening during NCS as follows:
The strong contractions of the ventricle walls are thought to cause a response in the mechanoreceptors, which misinterpret what is happening and send a message to the brain that the blood pressure is actually high. In response, the sympathetic portion of the cardiovascular center reduces its impulses to the heart and blood vessels while the parasympathetic division increases its impulses (Grubb & McMann, 2001, p. 61-62). This abnormal nervous system reflex causes the heart to slow and the blood vessels to dilate (open up), further lowering blood pressure (North American Society of Pacing and Electrophysiology, 1999). Because of this faulty adjustment, NCS patients may experience intermittent fainting.
A 2004 research publication suggests patients may awaken from sleep with symptoms of forthcoming neurocardiogenic syncope (Krediet, Jardine, Cortelli, Visman & Wieling, 2004). This suggestion may seem to contradict current teachings on this disorder. However, research shows that transient autonomic mechanisms that predispose to vasovagal syncope may occur during sleep (Shneerson, 2000, p. 1-15).
Findings from a 2008 neurocardiogenic syncope study seem to contradict current beliefs regarding what happens during a fainting episode as well. The results did not show an increase in ventricular contractility before tilt-induced syncope, or in presence of a valuable increase of sympathetic activity. Instead, the researchers observed a reduction of atrial contractility, which they believe may be a contributory component in the pathogenesis of vasovagal syncope .
There are several other factors that may be contributory components in the pathogenesis of vasovagal syncope as well. Differential changes in plasma levels of epinephrine, renin, endothelin, vasopressin, cortisol, prolactin, beta endorphins and substance P have been reported by some investigators either prior to or during a syncopal episode in patients with vasovagal syncope (Ellenbogen, Morillo, Wood, Gilligan, Eckberg & Smith, 1997). Further research has shown that galanin may play a role in one's ability to adapt to orthostatic stress. Patients may have a genetic susceptibility to NCS as well.
Some researchers have suspected that serotonin might be involved in the pathogenesis of NCS. Studies in animals have shown that the withdrawal of sympathetic impulses correlates with a higher level of serotonin being present in the central nervous system, the brain and the spinal cord (Grubb & McMann, 2001, p. 57). However a later study of NCS patients found no differences in serotonin activity at the time of fainting, but did show a lower serotonin level in patients during the early phase of tilt table testing (Mitro, Hijova & Mudrakova, 2006).
Another study showed that young women who had vasovagal syncope with a positive tilt test result had a greater sensitivity to insulin. Insulin, in addition to its known metabolic effects, has sympatho-excitatory and vasodilatory actions on muscular blood vessels. The authors of this study conclude that insulin hypersensitivity could be one of the predisposing factors for vasovagal episodes (Ruiz, Calvar, Hermes, Rivadeneira, Bengolea, Chirife, Tentori & Gelpi, 2003).
How is NCS diagnosed?
Tilt table testing is often used to diagnose NCS. However, tilt table testing can have false-negative and false-positive results (Levine, 1999).
How is NCS treated?
There are a variety of non-pharmacutical methods used to control and prevent neurocardiogenic syncope. No single therapy has been found to be effective in all patients. Non-pharmacutical therapies used to treat NCS include the following:
Cardioneuroablationreportedly has helped some neurocardiogenic syncope patients, although the study reporting this was small and patients had only been followed up for 9 months at the time of publishing (Pachon, Pachon, Pachon, Lobo, Pachon, Vargas & Jatene, 2005). Further investigation is warranted.
Counter-maneuvers may help some patients with neurocardiogenic syncope. Research has shown that physical counterpressure maneuvers are a risk-free, effective, and low-cost treatment for patients with vasovagal syncope and recognizable prodromal symptoms, and should be advised as first-line treatment in these patients (van Dijk, Quartieri, Blanc, Garcia-Civera, Brignole, Moya & Wieling, 2006).
Isometric arm counter-pressure maneuvers can increase systolic blood pressure and prevent fainting in some patients with NCS (Brignole, Croci, Menozzi, Solano, Donateo, Oddone, Puggioni & Lolli, 2002). Patients can perform isometric arm counter-pressure maneuvers by gripping one had with the other and pushing both arms away from their chest.
Leg crossing combined with muscle tensing at the onset of prodromal symptoms can postpone, and in some instances prevent, vasovagal syncope (Krediet, van Dijk, Linzer, van Lieshout & Wieling, 2002).
Sitting with the head between the knees often is an effective means of preventing syncope (Mathias, 2003).
One patient has reported success in warding off a fainting episode by gently but briskly stepping in place for a short time, bringing the knees a little upward and puffing out the exhale with each rep. Pumping the arms and fists during this counter-maneuver has helped her as well.
Increasing dietary salt and fluid intake may help prevent symptoms associated with neurocardiogenic syncope (Bloomfield, 2002).
Orthostatic self-training and tilt training may help select patients with NCS (Abe, Kondo, Kohshi, Nakashima, 2002). It is of greatest benefit to younger patients and those who faint frequently (Zeng, Ge, Zhang, Wang, & Guo, 2008). Orthostatic self-training involves standing against a wall, without moving, twice a day for a planned duration of up to 30 minutes. The results of orthostatic self-training studies have been mixed, with one study concluding it ineffective in reducing the positive response rate of head-up tilt test in patients with recurrent neurally mediated syncope (On, Park, Huh, & Kim, 2007).
Tilt training involves inclining patients on a tilt table each day. Some patients have to continually be inclined for this therapy to be effective. This therapy will not be effective in all patients. However, one study showed that in 19 patients who abandoned tilt training after about 1 year, none of them reported fainting during daily life. The authors of this study hypothesize that the disturbed autonomic reflex activity may have been restored in these patients (Reybrouck, Heidbuchel, Van De Werf & Ector, 2002).
Paced breathing may help to prevent vasovagal syncope induced by head-up tilt test. Researchers who studied the effects of paced breathing believe respiratory training could be useful in the prevention of vasovagal syncope (Jauregui-Renaud, Marquez, Hermosillo, Sobrino, Lara, Kostine & Cardenas, 2003).
Removal or avoidance of agents that predispose to hypotension or dehydration can lessen the occurance of neurocardiogenic syncope (Bloomfield, 2002). Situations that can predispose an individual to syncope are listed on the POTS Place "What to Avoid" page.
There are a variety of medications and medical treatments that may help prevent neurocardiogenic syncope as well. These include the following:
ACE inhibitors may prevent NCS, presumably through inhibition of sympathetic system activation and the peripheral hypotensive effect (Zeng, Zhu, Liu, Hu, Wang, Yang, Wang, He & Tan, 1998).
Alpha-agonists increase venous tone and decrease pooling, which may prevent activation of mechano-receptors. They also counteract the arteriolar vasodilation produced by the triggering of the vasovagal reflex (Raviele, Themistoclakis & Gasparini, 1996, p. 115). Midodrine is an example of an alpha-agonist that is used to treat NCS. Midodrine has been shown to significantly improve orthostatic tolerance during head-up tilt in patients with recurrent neurally mediated syncope (Kaufmann, Saadia & Voustianiouk, 2002). Researchers have also found Midodrine to be effective in both treating and preventing vasovagal syncope in children (Qingyou, Z., Junbao, D. & Chaoshu, T., 2006).
Beta blockers have been reported in many studies to be effective in treating neurocardiogenic syncope. Presumably, these agents exert their effects through their negative inotropic actions, which are felt to diminish the degree of cardiac mechano-receptor activation or by acting elsewhere to oppose the high levels of circulating epinephrine (Raviele, Themistoclakis & Gasparini, 1996, p. 114). However, studies of the efficacy of beta blockers in treating NCS have had mixed results. One study showed that propranolol, nadolol and placebo were all equally effective in treating vasovagal syncope (Flevari, Livanis, Theodorakis, Zarvalis, Mesiskli & Kremastinos, 2002). The physicians conducting this study concluded that beta blockers are no better than placebo at reducing neurocardiogenic syncope.
Another study showed nonselective beta blockers to be more effective than beta-1-selective blockers in preventing tilt-induced syncope (Dendi & Goldstein, 2002).
Calcium Channel Blockers may be effective in some patients with NCS. However, in a study comparing verapamil (a calcium channel blocker) to metoprolol (a beta blocker), verapamil was found to be less effective in the management of neurocardiogenic syncope (Jhamb, Singh, Sharda, Kaul, Goel, Talwar & Wasir, 1996).
Disopyramide has negative inotropic and anticholinergic effects that may be potentially beneficial in preventing vasovagal syncope by decreasing ventricular contractibility and counteracting parasympathetic activity (Raviele, Themistoclakis & Gasparini, 1996, p. 114).
Fludrocortisone is sometimes used to prevent neurocardiogenic syncope. There is considerable clinical experience and a consensus suggesting that fludrocortisone is effective (Bloomfield, 2002).
Pacemakers are a somewhat controversial treatment for neurocardiogenic syncope. Many studies have suggested the efficacy of pacemakers. However, a double-blind randomized trial showed that pacing therapy did not reduce the risk of recurrent syncope in patients with vasovagal syncope. The authors of this study concluded that pacemaker therapy should not be recommended as a first-line therapy for patients with recurrent vasovagal syncope (Connolly, Sheldon, Thorpe, Roberts, Ellenbogen, Wilkoff & Morillo, 2003).
Scopolamine may be effective in reducing the high vagal tone that occurs during syncopal episodes (Raviele, Themistoclakis & Gasparini, 1996, p. 115).
Serotonin Reuptake Inhibitors may prevent NCS by reducing the sympathetic impulses that signal the heart to contract more strongly (Grubb & McMann, 2001, p. 115).
Theophylline is an adenosine receptor blocker. It may prevent NCS, although patients sometimes discontinue theophylline because of adverse reactions (Nelson, Stanley, Love, Coyne & Schaal, 1991). Theophylline is not generally used as a first line treatment for NCS.
Patients sometimes need a combination of medications to prevent recurrent neurocardiogenic syncope.
To read more on NCS, please visit our neurocardiogenic syncope links page.
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