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| {{Neurocardiogenic Syncope}} | | '''For patient information on this page, click [[Neurocardiogenic syncope (patient information)|here]]''' |
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| | {{Neurocardiogenic syncope}} |
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| ==Pathophysiology== | | ==[[Neurocardiogenic syncope overview|Overview]]== |
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| *[[Neurocardiogenic Syncope]] is defined as a syndrome in which triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral vasodilation.
| | ==[[Neurocardiogenic syncope pathophysiology|Pathophysiology]]== |
| *It is caused by an abnormal or exaggerated autonomic response to various stimuli which results from excessive autonomic reflex activity, which shows as abnormal vascular tone and heart rate. In contrast, [[Orthostatic Hypotension]] is a failure of the autonomic reflex response.
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| ==Symptoms== | | ==[[Neurocardiogenic syncope epidemiology and demographics|Epidemiology & Demographics]]== |
| *Because vasovagal syncope may be precipitated by the sight of blood, loss of blood, sudden stressful or painful experiences, surgical manipulation, or trauma, a history of childhood syncope may provide a clue to the cause of vasovagal syncope in adults.
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| *Most patients have a prodome such as nausea, diaphoresis, lightheadedness, blurred vision, headaches, palpitations, paraesthesia, and pallor which usually occur in the upright position and resolve almost immediately when the patient assumes the supine position.
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| *Patients may also complain of a “washed out” and tired feeling.
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| ===Physical Examination=== | | ==[[Neurocardiogenic syncope risk factors|Risk Factors]]== |
| THe physical examination is unremarkable in 50% of patients.
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| ==Treatment== | | ==[[Neurocardiogenic syncope causes|Causes]]== |
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| *Infrequent episodes of vasovagal syncope that are preceded by a warning prodrome probably do not require any intervention besides counseling and observation. Attention to hydration and salt intake may suffice.
| | ==[[Neurocardiogenic syncope natural history|Natural History, Prognosis & Complication]]== |
| *Beta blockers are preferred as initial treatment but have not been demonstrated as effective in a RCT. The [[Prevention of Syncope Trial]] showed that metoprolol was overall ineffective in preventing syncope.
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| *In patients with borderline low blood pressure who may be subject to symptomatic orthostasis, fludrocortisone, midodrine, and compression hose are often used initially.
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| **Midodrine (ProAmantine 2.5-10 TID), an alpha agonist has been shown to be effective in several randomized controlled clinical trials. Side effects include nausea and supine hypertension.
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| **Fludrocortisone 0.1 mg/ Day, a mineralocorticoid that promotes renal reabsorption of sodium to cause increased blood volume has been used in the treatment of vasodepressor syncope in both children and adults. Caution is needed in elderly patients because they poorly tolerate the drug and there is a risk of hypertension, cardiac failure, and edema.
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| *Scopolamine, an anticholinergic agent, has central nervous system depressant effects and has been used successfully in some patients with syncope
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| *Selective serotonin reuptake inhibitors (Paxil 20mg/ Day) selectively block serotonin, which has been shown to induce vagally mediated bradycardia and blood pressure lowering.
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| *Pyridostigmine (Mestinon 60mg po BID), an acetylcholinesterase inhibitor which increases acetylcholine levels at the autonomic ganglia. It prevents a drop in blood pressure without causing supine hypertension. Demonstrated to be effective in POTS and orthostatic Hypotension. Can be used in conjuction with Midrodrine.
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| *In regards to pacing, in the '''VPS II Study''', 100 patients whoo were > 19 years of age who had a history of recurrent vasovagal syncope with 6 episodes of syncope ever or 3 episodes in the past 2 years, and a positive result on the head-up tilt table test (TTT) with a heart rate × blood pressure product < 6000/min × mm Hg were randomized to receive dual chamber pacing with rate drop. The results demonstrated that fewer patients in the DDD group than the ODO group had syncope during follow-up, but the difference did not reach statistical significance. Compared with ODO, the relative risk reduction in time to syncope with DDD was 30% (95% CI −33% to 63%). The number of pacemaker complications was similar between the DDD and ODO groups (10 vs 9 complications).
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| ==ACC / AHA Guidelines- Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT) <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>== | | ==[[Neurocardiogenic syncope differentiating from other diseases|Differentiating Neurocardiogenic Syncope From Other Diseases]]== |
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| ===Class I===
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| 1. Permanent [[pacemaker|pacing]] is indicated for recurrent [[syncope]] caused by spontaneously occurring [[carotid sinus]] stimulation and [[carotid sinus]] pressure that induces [[ventricular asystole]] of more than 3 seconds. ''(Level of Evidence: C)''
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| ===Class IIa=== | | ==Diagnosis== |
| 1. Permanent [[pacemaker|pacing]] is reasonable for [[syncope]] without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. ''(Level of Evidence: C)''
| | [[Neurocardiogenic syncope symptoms|History & Symptoms]] | [[Neurocardiogenic syncope physical examination|Physical Examination]] | [[Neurocardiogenic syncope electrocardiogram|Electrocardiogram]] | [[Neurocardiogenic syncope chest x-ray|Chest X-Ray]] | [[Neurocardiogenic syncope tilt table testing|Tilt table test]] | [[Neurocardiogenic syncope echocardiography|Echocardiography]] | [[Neurocardiogenic syncope cardiac catheterization|Cardiac Catheterization]] |
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| ===Class IIb=== | | ==Treatment== |
| 1. Permanent [[pacemaker|pacing]] may be considered for significantly symptomatic neurocardiogenic [[syncope]] associated with [[bradycardia]] documented spontaneously or at the time of tilt-table testing. ''(Level of Evidence: B)''
| | ====[[Neurocardiogenic syncope medical treatment|Medical Therapy]]==== |
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| ===Class III=== | |
| 1. Permanent [[pacemaker|pacing]] is not indicated for a hypersensitive cardioinhibitory response to [[carotid sinus]] stimulation without symptoms or with vague symptoms. ''(Level of Evidence: C)''
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| 2. Permanent [[pacemaker|pacing]] is not indicated for situational vasovagal [[syncope]] in which avoidance behavior is effective and preferred. ''(Level of Evidence: C)''}}
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| ==Sources== | |
| * The ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities <ref name="Epstein"> Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207 </ref>
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| ==References== | | ====[[Neurocardiogenic syncope pacemaker therapy|Pacemaker Therapy]]==== |
| {{reflist|2}}
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| # Neurocardiogenic syncope. Carol Chen-Scarabelli, Tiziano M Scarabelli. BMJ 2004;329:336–41
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| # Brignole M, Alboni P, Benditt D, Bergfeldt L, Blanc JJ, Bloch Thomsen PE, et al for the Task Force on Syncope, European Society of Cardiology.Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J 2001;22:1256-306.
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| # Vasovagal Syncope. Alexis M. Fenton, MD; Stephen C. Hammill, MD; Robert F. Rea, MD; Phillip A. Low, MD; and Win-Kuang Shen, MD. Ann Intern Med. 2000;133:714-725.
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| # Connolly SJ, Sheldon R, Thorpe KE, et al. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope: Second Vasovagal Pacemaker Study (VPS II): a randomized trial. JAMA. 2003;289:2224-9.
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| {{SIB}}
| | ==Related Chapters== |
| | *[[Vasovagal syncope]] |
| | *[[Postural orthostatic tachycardia syndrome]] |
| | *[[Dysautonomia]] |
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| | [[Category:Disease]] |
| [[Category:Cardiology]] | | [[Category:Cardiology]] |
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