Neurocardiogenic syncope

Pathophysiology

 * 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.
 * 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.

Symptoms

 * 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.
 * 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.
 * Patients may also complain of a “washed out” and tired feeling.

Treatment

 * 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.
 * 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.
 * In patients with borderline low blood pressure who may be subject to symptomatic orthostasis, fludrocortisone, midodrine, and compression hose are often used initially.
 * 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.
 * 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.
 * Scopolamine, an anticholinergic agent, has central nervous system depressant effects and has been used successfully in some patients with syncope
 * Selective serotonin reuptake inhibitors (Paxil 20mg/ Day) selectively block serotonin, which has been shown to induce vagally mediated bradycardia and blood pressure lowering.
 * 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.
 * 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).

==ACC / AHA Guidelines- Permanent Pacing in Hypersensitive Carotid Sinus Syndrome and Neurocardiogenic Syncope (DO NOT EDIT) == {{cquote|

Class I
1. Permanent 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)

Class IIa
1. Permanent pacing is reasonable for syncope without clear, provocative events and with a hypersensitive cardioinhibitory response of 3 seconds or longer. (Level of Evidence: C)

Class IIb
1. Permanent 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)

Class III
1. Permanent pacing is not indicated for a hypersensitive cardioinhibitory response to carotid sinus stimulation without symptoms or with vague symptoms. (Level of Evidence: C)

2. Permanent pacing is not indicated for situational vasovagal syncope in which avoidance behavior is effective and preferred. (Level of Evidence: C)}}