Common Cause Of Syncope Research Articles

Diagnosis and management of neurally mediated syncope and related conditions in adolescents.

Our knowledge of the etiologies of syncope and presyncope has been rapidly expanding along with an awareness that syncope, previously considered a universally benign event, does require evaluation. Syncope during adolescence can be caused by a variety of conditions including: neurologic, cardiac (excluding arrhythmias), arrhythmogenic, metabolic, and psychiatric conditions (Table 1) (1–10). The most common cause of syncope (at least 50%) appears to be neurally mediated syncope (11–14). Neurally mediated syncope (NMS), defined as the transient loss of blood flow to the brain secondary to hypotension and bradycardia, is emerging as a significant and potentially disabling condition for many adolescents. This condition may produce a wide variety of symptoms that include, but are not limited to, fatigue, dizziness, abdominal discomfort, muscle or joint pain, decreased mental concentration, and syncope (15). Syncope may occur without warning, thus precipitating trauma or death if the adolescent is engaged in an activity such as driving a vehicle or standing on a ladder. Linzer et al. (16) have shown that people with recurrent syncope have significant impairment, both of psychosocial and physical functioning. Teenagers may miss a great deal of school, work, and social activities owing to incapacitating symptoms, misdiagnosis, or ineffective treatment. Furthermore, lack of preparation of school personnel or employers to feel comfortable in assisting the adolescent with management of their symptoms while at school or work may also keep them from normal adolescent activities. Because these symptoms can be associated with a variety of conditions, an expensive and exhaustive evaluation is generally done. An empiric knowledge base is building to support NMS as an easily diagnosed and treatable condition. This article will focus on the etiologies of syncope and presyncope that can be diagnosed by tilt-table testing and describe an appropriate assessment, evaluation, and intervention in a cost-effective yet inclusive manner.

The pathophysiology of common causes of syncope

The pathophysiology of common causes of syncope

Potential risk of vasovagal syncope for motor vehicle driving

Vasovagal syncope is the most common cause of syncope, but its risk for driving remains uncertain. We analyzed the clinical characteristics of patients who had syncope during driving and subsequently underwent the head-up tilt test (HUTT). Of the 245 consecutive patients undergoing HUTT, 23 (9%) had ≥1 episode of syncope during driving. HUTT was positive in 19 (group A) and negative in 4 (group B) patients. No patient had structural heart disease. In group A, the driving incident occurred on the first syncope in 3 patients, and the other 16 patients had 1 to 4 episodes of prior syncope not associated with driving. In group B, the driving incident occurred on the first syncope in 1 patient, and the other 3 patients had prior syncope (3 episodes in each) not associated with driving. Seven group A and 1 group B patients had 2 syncope-related driving incidents, and the remaining patients had only 1 syncope-related driving incident. The syncope-related driving incidents caused personal injury in 7 group A and 2 group B patients. One incident in 1 group A patient caused the death of another driver. After HUTT, all but 1 patient in group A received medical treatment and only 1 patient in group B received empirical β-blocker therapy. During the follow-up of 51 ± 26 months, 1 patient died and another was lost to follow-up. Of the remaining patients, 4 patients had recurrence of syncope and 2 patients had presyncope in group A. One of these patients had another syncope-related driving incident. No group B patient had syncope recurrence. A second etiology of syncope was never found in any patient. We conclude that vasovagal syncope during driving is not uncommon in patients referred for syncope evaluation. Early medical attention to patients with vasovagal syncope may help reduce syncope-related driving incidents.

Driving safety among patients with neurocardiogenic (vasovagal) syncope.

Neurocardiogenic syncope is one of the most common causes of syncope. However, the important issue of driving related injury due to syncope in this population is not well defined. Risk of injury due to syncope while driving and driving behavior was evaluated in 155 consecutive patients (92 women and 63 men; mean age 49 +/- 19 years) with history of syncope in whom hypotension and syncope or presyncope could be provoked during head-up tilt testing. Patients with syncope and positive head-up tilt table test were treated with pharmacological therapy. All participants were asked to fill out a detailed questionnaire regarding any driving related injuries and their driving behavior before tilt table testing and during follow-up. Prior to head-up tilt testing two patients had syncope while driving, and one of these patients had syncope related injury during driving. The mean duration of syncopal episodes was 50 +/- 14 months (range 12-72 months). Of the 155 patients, 52 (34%) had no warning prior to syncope, while 103 (6%) had warning symptoms such as dizziness prior to their clinical syncope. Following a diagnosis of neurocardiogenic syncope established by head-up tilt testing, six patients stopped driving on their own. During a median follow-up of 22 months recurrent syncope occurred in five (3.2%) patients. No patient had syncope or injury during driving. In conclusion, syncope and injury while driving in patients with neurocardiogenic syncope is rare. The precise mechanism of this is unclear but may be related to posture during driving. Consensus among the medical community will be needed to provide specific guidelines in these patients.

Diagnosis and management of neurocardiogenic syncope.

The medical term syncope is derived from the Greek word "synkoptein," the original meaning of which was "to cut short". Because it is both a symptom and a sign, the physician may often find the evaluation of syncope a difficult and frustrating endeavor. Over the course of the past decade it has become apparent that transient alterations in autonomic nervous system activity, resulting in hypotension and bradycardia, are common causes of syncope. At the same time it has become apparent that these are a heterogenous group of disorders which, while sharing some characteristics, are nonetheless distinct maladies. This article attempts to briefly review our current understanding of these disorders and suggests guidelines on their diagnosis and management.

VALUE AND LIMITATIONS OF ELECTROPHYSICAL TESTING FOR SYNCOPE

Syncope is by definition a transient event, and its cause has usually resolved by the time the patient is examined. Electrophysiologic testing provides a method for assessing a patient's risk for future arrhythmias based on the known sensitivity and specificity of the analyses of sinus node function, atrioventricular conduction, and responses to programmed atrial and ventricular stimulation. Interpretation of these data must always be made in the context of the patient's total clinical situation.

VALUE AND LIMITATIONS OF NONINVASIVE ASSESSMENT OF SYNCOPE

The noninvasive assessment of patients who present with syncope is based on a thorough, complete history and physical examination. The history requires close attention to precipitating events and the description of the spell. Often, patients are poor historians with regard to symptoms leading up to and following the episode of syncope. Therefore, it is important to interview individuals who observed the spell to improve the accuracy of the history and sort out whether or not the spell was due to cardiogenic syncope, vasodepressor syncope, or a neurologic disorder. Carotid sinus massage is a useful procedure that can be performed during the routine physical examination, identifying patients who are at increased risk for carotid sinus syncope because of hypersensitivity of the carotid sinus. The clinician must be careful to attribute the clinical syncope to carotid sinus hypersensitivity only when the spell induced at the time of carotid massage reproduces the clinical spell. Routine laboratory tests are commonly performed, although the blood tests rarely yield information to confirm the cause of syncope. The routine ECG is often helpful identifying abnormalities of rhythm, conduction, or morphology that give a clue as to the cause for the patient's syncope. The most helpful aspect of ECG recording is to obtain a recording during an episode of syncope when exact correlation can be made between the ECG findings and the patient's symptoms. Recording the ECG during the spell can be achieved using 24-hour ambulatory monitoring, an event recorder, or a memory loop recorder. Twenty-four-hour ambulatory monitoring is useful in patients who have frequent spells that would be expected to be recorded during 1 or 2 days of monitoring. These individuals need to have a non-life-threatening spell and therefore be safe to evaluate as an outpatient. The event recorder and loop memory recorder have proved extremely helpful in evaluating spells that occur too infrequently to be recorded by 24-hour or 48-hour ambulatory monitoring. The nature of these recording devices does require that the patient or a companion be able to activate the monitor at the time of symptoms. If a patient experiences syncope but is unable to activate the device, the important information as to what the rhythm was doing at the time of symptoms is lost. The implantable loop recorder should prove to be uniquely advantageous by allowing extended ECG recording with the device activated by the patient or companion recording 20 minutes before and 4 minutes after device activation. Signal-averaged electrocardiography is most helpful in assessing patients with ischemic heart disease with a substrate capable of supporting a reentrant ventricular arrhythmia. This test should be used in combination with other historical or laboratory predictors of arrhythmic events such as history of myocardial infarction or abnormal ventricular function assessed by echocardiography. In this setting, the signal-averaged ECG helps to identify patients at increased risk for ventricular tachycardia as the cause of syncope who thus may benefit from electrophysiologic testing.

Current trends in etiology, diagnosis, and management of neurocardiogenic syncope.

Recurrent episodes of unexplained syncope are among the most frequent of complaints referred to physicians for evaluation. Traditional methods of evaluation were both time consuming and expensive and left many patients without a diagnosis. Although neurocardiogenically mediated episodes of hypotension and bradycardia were felt to be a common cause of syncope, this was traditionally a diagnosis of exclusion. The emergence of head-upright tilt-table testing has provide a valuable method for identifying individuals predisposed to neurocardiogenic syncope and has also allowed for a better understanding of this phenomena. This article reviews the pathophysiology of neurocardiogenic syncope, the use of head-upright tilt-table testing in its diagnosis, and the potential therapies used to prevent recurrences.

Head-upright tilt table testing in evaluation of recurrent, unexplained syncope

Recurrent syncope is one of the most common problems referred to the pediatric neurologist for evaluation. Traditional evaluations are time consuming and expensive, and leave 40% of patients without a precise diagnosis. Vasovagal syncope has been believed to be a common cause of syncope; however, no reliable diagnostic modality has been available to confirm this theory. Head-upright tilt table testing has recently emerged as a useful tool in the evaluation and management of recurrent, unexplained syncope. In this review, we present the pathophysiologic mechanisms of vasovagal syncope and relate them to the reflexes triggered during head-upright tilt table testing. Additionally, we review the clinical data on the uses of this test in unexplained syncope, suggest a practical testing protocol, and elaborate potential therapeutic modalities that can be employed to prevent further episodes. Head-upright tilt table testing will likely become a standard test employed by both adult and child neurologists.

Medically unexplained syncope: Relationship to psychiatric illness

The purpose of this article is to review the literature and present new data concerning the relationship between psychiatric disorders and unexplained syncope. Several case series are presented of patients with syncope in whom psychiatric structured interviews were undertaken, tilt-table (physiologic) testing was performed, and health-related quality of life was measured. Patients seen in a syncope specialty clinic underwent structured psychiatric interviews in addition to in-depth medical evaluations. Tilt-table testing was performed on a separate series of patients to determine susceptibility to syncope during the orthostatic challenge of head-up tilt; in some cases, tilt studies included simultaneous electroencephalographic (EEG) monitoring and cerebral blood flow measurements. Formal functional status assessment was carried out using the Sickness Impact Profile, the Symptom Check List 90, and the Medical Outcomes Study Short-Form 36. Psychiatric disorders (in particular, panic disorders and major depression) were a common cause of syncope (24–31% of syncope patients). Tilt table studies showed several physiologic profiles in syncope: (a) a typical vasovagal (hypotension-bradycardia) response, (b) a “psychosomatic” response (fainting with normal vital signs), and (c) a gradual decline in blood pressure (dysautonomic response). EEG and cerebral blood flow measurements in three patients with the psychosomatic response to tilt were normal during fainting. Functional status measurements showed serious impairment in two series of syncope patients. Conclusions were as follows: (a) Psychiatric disorders are common in syncope. (b) Tilt-table methodology may elucidate underlying mechanisms of syncope in these subjects. (c) Syncope can seriously disrupt a patient's life and result in important psychosocial sequelae. (d) There is an intimate relationship between unexplained syncope and psychiatric illness, mandating a combined medical and psychiatric approach to such patients.

Tilt Test for Diagnosis of Unexplained Syncope in Pediatric Patients

Thirty-five teenage patients with a history of presyncope or syncope underwent a passive head-up tilting to reproduce symptoms of syncope. If tilting alone did not induce syncope, isoproterenol infusion was given to increase heart rate to 150 to 160 beats per minute. In 80% of patients with a history of syncope, identical symptoms could be reproduced during tilting: an abrupt fall in blood pressure combined with profound nodal bradycardia, ranging from 32 to 86 beats per minute. These symptoms were quickly reversed by returning the patient to the supine position. For patients with frequent occurrences of syncope, especially when there was a history of trauma sustained during these episodes, a therapeutic regimen of either beta blockers or 9 alpha-fluorocortisol was begun. The mechanisms of this common cause of syncope in childhood is neurocardiogenic in response to venous pooling and catecholamine-induced tachycardia. The tilt test is an excellent and cost-effective test for the workup of unexplained syncope in childhood.

Provocation of bradycardia and hypotension by isoproterenol and upright posture in patients with unexplained syncope.

Neurally mediated hypotension and bradycardia are believed to be common causes of syncope. We used the "upright-tilt test" (duration, less than or equal to 10 minutes) with or without an infusion of exogenous catecholamine (isoproterenol [1 to 5 micrograms per minute], given intravenously) to elicit bradycardia, hypotension, or both in 24 patients with recurrent syncope and in 18 control subjects. A conventional electrophysiologic test performed before the tilt test was positive in 9 of the 24 patients, revealing arrhythmias that may have caused recurrent syncope, but was negative and thus nondiagnostic in 15 patients. The tilt test alone (i.e., without isoproterenol) induced symptomatic bradycardia or hypotension in 1 of the 9 patients with positive electrophysiologic tests (11 percent), 4 of the 15 patients with negative electrophysiologic tests (27 percent), and none of the controls. When the isoproterenol infusion was administered during the tilt test, 9 of the 11 patients with negative electrophysiologic and tilt tests had syncope, marked slowing of the heart rate, and hypotension. In contrast, isoproterenol was associated with tachycardia and only a slight decline in arterial pressure in the 8 remaining patients with positive electrophysiologic tests and the 18 control subjects, and syncope developed in only 1 of the 8 patients with positive electrophysiologic tests and negative tilt tests (13 percent) and 2 of the 18 control subjects (11 percent). We conclude that an isoproterenol infusion administered in conjunction with the upright-tilt test may be useful for identifying susceptibility to neurally mediated recurrent syncope.