Evaluation of syncope

Though relatively common, syncope is a complex presenting symptom defined by a transient loss of consciousness, usually accompanied by falling, and with spontaneous recovery. Syncope must be carefully differentiated from other conditions that may cause a loss of consciousness or falling. Syncope can be classified into four categories: reflex mediated, cardiac, orthostatic, and cerebrovascular. A cardiac cause of syncope is associated with significantly higher rates of morbidity and mortality than other causes. The evaluation of syncope begins with a careful history, physical examination, and electrocardiography. Additional testing should be based on the initial clinical evaluation. Older patients and those with underlying organic heart disease or abnormal electrocardiograms generally will need additional cardiac evaluation, which may include prolonged electrocardiographic monitoring, echocardiography, and exercise stress testing. When structural heart disease is excluded, tests for neurogenic reflex-mediated syncope, such as head-up tilt-table testing and carotid sinus massage, should be performed. The use of tests such as head computed tomography, magnetic resonance imaging, carotid and transcranial ultrasonography, and electroencephalography to detect cerebrovascular causes of syncope should be reserved for those few patients with syncope whose history suggests a neurologic event or who have focal neurologic signs or symptoms.     

To stand on one's own legs

A fundamental human expectation is to stand upright. This exposes the cardiovascular system to gravitational forces, with a fall in pressure above heart level exposing organs such as the brain to impaired perfusion if adequate adaptive mechanisms are not activated. The autonomic nervous system plays an important role in the initial response to standing upright, and can be affected by several disorders, some rare, some common. Autonomic failure can result in orthostatic hypotension with hypoperfusion of vital organs, causing a variety of symptoms including syncope. Thus, it is important to recognise orthostatic hypotension, determine its aetiology, evaluate and treat it. Intermittent autonomic dysfunction (such as neurally mediated syncope without chronic neurogenic failure) also results in falls and syncope; various forms include the 'common faint' (vasovagal syncope) and carotid sinus hypersensitivity (especially in the elderly). Orthostatic intolerance without orthostatic hypotension is increasingly recognised as due to an autonomic disturbance. New techniques are helping to unravel the functional anatomy of cerebral autonomic centres and their pathways in the causation of orthostatic intolerance.     

Management of syncope in adults: an update

Syncope is a clinical syndrome characterized by transient loss of consciousness and postural tone that is most often due to temporary and spontaneously self-terminating global cerebral hypoperfusion. A common presenting problem to health care systems, the management of syncope imposes a considerable socioeconomic burden. Clinical guidelines, such as the European Society of Cardiology Guidelines on Management of Syncope, have helped to streamline its management. In recent years, we have witnessed intensive efforts on many fronts to improve the evaluation process and to explore therapeutic options. For this update, we summarized recent active research in the following areas: the role of the syncope management unit and risk prediction rules in providing high-quality and cost-effective evaluation in the emergency department, the implementation of structured history taking and standardized guideline-based evaluation to improve diagnostic yield, the evolving role of the implantable loop recorder as a diagnostic test for unexplained syncope and for guiding management of neurally mediated syncope, and the shift toward nonpharmacological therapies as mainstay treatment for patients with neurally mediated syncope. Syncope is a multidisciplinary problem; future efforts to address critical issues, including the publication of clinical guidelines, should adopt a multidisciplinary approach.     

Stepwise Evaluation of Unexplained Syncope in a Large Ambulatory Population

Background: Up to 60% of syncopal episodes remain unexplained. We report the results of a standardized, stepwise evaluation of patients referred to an ambulatory clinic for unexplained syncope.
Methods and Results: We studied 939 consecutive patients referred for unexplained syncope, who underwent a standardized evaluation, including history, physical examination, electrocardiogram, head-up tilt testing (HUTT), carotid sinus massage (CSM) and hyperventilation testing (HYV). Echocardiogram and stress test were performed when underlying heart disease was initially suspected. Electrophysiological study (EPS) and implantable loop recorder (ILR) were used only in patients with underlying structural heart disease or major unexplained syncope. We identified a cause of syncope in 66% of patients, including 27% vasovagal, 14% psychogenic, 6% arrhythmias, and 6% hypotension. Noninvasive testing identified 92% and invasive testing an additional 8% of the causes. HUTT yielded 38%, CSM 28%, HYV 49%, EPS 22%, and ILR 56% of diagnoses. On average, patients with arrhythmic causes were older, had a lower functional capacity, longer P-wave duration, and presented with fewer prodromes than patients with vasovagal or psychogenic syncope.
Conclusions: A standardized stepwise evaluation emphasizing noninvasive tests yielded 2/3 of causes in patients referred to an ambulatory clinic for unexplained syncope. Neurally mediated and psychogenic mechanisms were behind >50% of episodes, while cardiac arrhythmias were uncommon. Sudden syncope, particularly in older patients with functional limitations or a prolonged P-wave, suggests an arrhythmic cause.     

Evaluation of syncope: focus on diagnosis and treatment of neurally mediated syncope

Syncope, defined as a transient loss of consciousness secondary to global cerebral hypoperfusion, is common in the general population. The single most helpful “test” in the evaluation of patients with syncope is a thoughtful history, with recent evidence that structured histories are remarkably effective in arriving at a diagnosis. In addition to the history, physical examination, and electrocardiogram, arriving at a diagnosis of syncope can involve monitoring and provocative strategies. The majority of patients with syncope have neurally mediated syncope and a favourable prognosis. The management of neurally mediated syncope continues to largely revolve around education, avoidance of triggers, reassurance, and counter-pressure maneuvers. The evidence surrounding medical therapy in vasovagal syncope is not strong to date. Pacemaker therapy is reasonable in older patients with recurrent, unpredictable syncope with pauses, but should be considered as a last resort in younger patients.     

Tilt table testing,methodology and practical insights for the clinic

Tilt table testing (TTT) has been used for decades to study short-term blood pressure (BP) and heart rate regulation during orthostatic challenges. TTT provokes vasovagal reflex in many syncope patients as a background of widespread use. Despite the availability of evidence-based practice syncope guidelines, proper application and interpretation of TTT in the day-to-day care of syncope patients remain challenging. In this review, we offer practical information on what is needed to perform TTT, how results should be interpreted including the Vasovagal Syncope International Study classification, why syncope induction on TTT is necessary in patients with unexplained syncope and on indications for TTT in syncope patient care. The minimum requirements to perform TTT are a tilt table with an appropriate tilt-down time, a continuous beat-to-beat BP monitor with at least three electrocardiogram leads and trained staff. We emphasize that TTT remains a valuable asset that adds to history building but cannot replace it, and highlight the importance of recognition when TTT is abnormal even without syncope. Acknowledgement by the patient/eyewitness of the reproducibility of the induced attack is mandatory in concluding a diagnosis. TTT may be indicated when the initial syncope evaluation does not yield a certain, highly likely, or possible diagnosis, but raises clinical suspicion of (1) reflex syncope, (2) orthostatic hypotension (OH), (3) postural orthostatic tachycardia syndrome or (4) psychogenic pseudosyncope. A therapeutic indication for TTT in the patient with a certain, highly likely or possible diagnosis of reflex syncope, may be to educate patients on prodromes. In patients with reflex syncope with OH TTT can be therapeutic to recognize hypotensive symptoms causing near-syncope to perform physical countermanoeuvres for syncope prevention (biofeedback). Detection of hypotensive susceptibility requiring therapy is of special value.     

Incidence and Predictors of Syncope in Paced Patients with Sick Sinus Syndrome

In spite of a normal pacemaker/unction, syncope still occurs in some patients with sick sinus syndrome (SSSJ. Causes often remain unknown. To identify predictors and etiologies of this bothersome symptom, we studied 507 patients who received atrial, ventricular, and dual-chamber pacemakers for SSS. During a mean follow-up of 62 ± 38 months, actuarial incidence of syncope was 3% at 1 year, 8% at 5 years, and 13% at 10 years. Causes were vasovagal (18%), orthostatic hypotension (25.5%), rapid atrial tachyarrhythmias (11.5%), ventricular tachycardia (5%), acute myocardial ischemia (2.5%), and pacemaker/lead malfunction (6.5%), In 13 patients (29.5%), syncope remained unexplained. The only preimplant predictor for syncope was syncope as primary indication for pacemaker implant. Electrocardiographic correlation with bradycardia was not a predictor of relief of syncope during the follow-up. In conclusion: (1) syncope in paced patients with SSS has multiple etiologies and may be multifactorial; (2) the only predictor of syncope after pacemaker implant is the occurrence of preimplant syncope as the main indication for pacing; (3) extensive Holier monitoring is not useful to document bradycardic origin of syncope nor to predict its recurrence; (4) SSS probably overlaps with other entities such as autonomic dysfunction, vasovagal syncope, carotid sinus hypersensitivity, and venous pooling, which would provide an explanation for recurrent syncope in patients with normal pacemaker function.     

The Use of Head-Upright Tilt Table Testing in the Evaluation and Management of Syncope in Children and Adolescents

Recurrent syncope in an otherwise healthy child or adolescent is a common anxiety provoking disorder. Vasovagally mediated hypotension and bradycardia are believed common, yet difficult to diagnose, causes of syncope in this age group. Upright tilt table testing has been suggested as a potential method to test for vasovagal episodes. This study evaluated the utility of this technique in the evaluation and management of recurrent syncope in children and adolescents. Thirty patients with recurrent unexplained syncope were evaluated by use of an upright tilt table test for 30 minutes, with or without an infusion of isoproterenol (1 to 3 micrograms/min given intravenously), in an attempt to produce hypotension, bradycardia, or both. There were 15 males and 15 females, mean age 14 +/- 6 years. Each of the tilt positive patients received therapy with either fluorohydrocortisone, beta blockers, or transdermal scopolamine. Syncope occurred in six patients (20%) during the base line tilt and in 15 patients (50%) during isoproterenol infusion (total positives 70%). All initially positive patients were rendered tilt negative by therapy. Over a mean follow-up period of 20 months, no further episodes have occurred. We conclude that tilt table testing is a useful and effective test in the evaluation of unexplained syncope in childhood.     

Neurally Mediated Syncopal Syndromes: Pathophysiological Concepts and Clinical Evaluation

The neurally mediated syncopal syndromes encompass a number of apparently related disturbances of reflex cardiovascular control characterized by transient inappropriate bradycardia and/or vasodilation of various arterial and venous beds. Certain of these syndromes (e.g., carotid sinus syndrome, postmicturition syncope) are encountered occasionally in clinical practice, whereas others are quite rare (e.g., swallow syncope). On the other hand, vasovagal syncope occurs so frequently, that as a group, the neurally mediated syncopal syndromes are among the most important causes of syncope. The pathophysiology of the neurally mediated syncopal syndromes is incompletely understood, but can be considered in terms of four basic elements: (1) the afferent limb; (2) central nervous system (CNS) processing; (3) the efferent limb; and (4) feedback loops. The afferent limb consists of several peripheral and CNS trigger sites and the associated connections to medullary cardiovascular control centers. CNS processing and efferent signals result in both bradycardia, which may be marked or relative, and vasodilatation. Failure of baroreceptor feedback controls to prevent hypotension is important in facilitating development of symptomatic hypotension. Head-up tilt table testing has become the diagnostic technique of choice for clinically assessing susceptibility to neurally mediated syncope, particularly of the vasovagal type. Most studies suggest that such testing discriminates relatively well between symptomatic patients and asymptomatic control subjects, of whom 10%–15% have a false-positive test result. Sensitivity of tilt table testing is more difficult to evaluate because there is no accepted diagnostic gold standard. However, sensitivity (measured against a classic presentation) has been estimated to range from 32%–85%, with most reports favoring the higher end of this range. Treatment strategies for neurally mediated syncope remain controversial. Many single episodes do not warrant treatment unless physical injury has occurred, or a high risk occupation or avocation is involved. Tilt test exposure alone may prove beneficial in educating patients with recurrent syncope to recognize warning signs of an imminent faint. Large controlled clinical studies have not been performed to test the efficacy of pharmacological therapy (e.g., β-adrenergic blockers, disopyramide, serotonin reuptake blockers, vasoconstrictors) or pacing therapy. Such studies may be difficult to undertake due to the variable frequency of spontaneous symptoms and apparent long periods of remission. Nonetheless, many investigators and clinicians have come to rely on these agents, and on tilt testing to guide treatment decisions. Studies employing careful correlation of long-term clinical follow-up with results of early and perhaps later repeat tilt studies are still needed.     

直立倾斜试验诊断不明原因晕厥的价值

目的探讨直立倾斜试验在不明原因晕厥诊断中的价值。方法不明原因晕厥患者366例,均行直立倾斜试验检查。结果直立倾斜试验阳性252例,阳性率68．9％;直立性不耐受综合征类型中以血管迷走性晕厥多见,其次为体位性心动过速、直立性低血压;血管迷走性晕厥中血管减压型比例女性高于男性（P〈O．05）;年龄≥60岁15例患者中直立倾斜试验阳性10例,均表现为血管迷走性晕厥;13例发生假性晕厥。结论直立倾斜试验阳性者并非为反射性晕厥,直立位3～45min发生晕厥的阳性患者,须结合年龄、性别及病史确诊是体位性晕厥或反射性晕厥。     

Recurrent Symptoms after Ventricular Pacing in Unexplained Syncope

We report clinical and hemodynamic data in two cases of recurrent syncope. Both patients received permanent demand ventricular pacing (VVI) for unexplained syncope. Both patients experienced recurrent syncope after pacemaker implantation. They later underwent 60 degrees head-up tilt testing, initially noninvasively and then with hemodynamic profile. A vasovagal response to tilt occurred with bradycardia and was complicated by the onset of ventricular pacing and retrograde atrioventricular conduction (RAVC) with hemodynamic deterioration and rapid reproduction of syncope. Limited intracardiac electrophysiological study (EPS) excluded atrioventricular (AV) conduction disease, sinus node disease, and carotid sinus syndrome, and confirmed RAVC. Both patients were upgraded to dual chamber pacing, DDI mode, with 50/80 rate hysteresis. One patient was asymptomatic at repeat tilt testing; the other experienced continued symptoms due to the vasodepressor component of vasovagal syncope. Cardiac pacing alone is ineffective treatment for this phenomenon, and no proven therapy is presently available. Ventricular pacing applied to patients with unexplained syncope may lead to an increase in or continuation of symptoms rather than an amelioration. There is a need for full investigation of such patients, which must include tilt testing, to allow for the most accurate diagnosis possible and guide the most appropriate therapy.     

Possible Involvement of Cerebral Hypoperfusion as a Trigger of Neurally-Mediated Vasovagal Syncope

It is well known that some patients with neurally mediated syncope have a feeling of aura before the onset of syncope. A case is reported in which cerebral dysfunction recorded by EEG was present before the onset of a vasovagal reaction. The vasovagal reaction, bradycardia and/or asystole, was preceded by abnormal EEG findings when the patient complained of feeling a headache, photophobia, and nausea. These findings suggest that cerebral hypoperfusion, such as with cerebral vasospasms, before the onset of bradycardia might be involved in the mechanism of neurally mediated syncope in patients with an aura.     

Is Home Orthostatic Self‐Training Effective in Preventing Neurally Mediated Syncope?

BACKGROUND: Repeated orthostatic stress may prove to be of benefit in the regulation of neurally mediated syncope. But the role of home orthostatic self-training is not established to prevent symptoms in patients with neurally mediated syncope. We performed a prospective and randomized study to evaluate the effectiveness of repeated home orthostatic self-training in preventing tilt-induced neurally mediated syncope. METHODS AND RESULTS: Fourty-two consecutive patients (24 males and 18 females, mean age 39 years, 16-68 years) with recurrent neurally mediated syncope were randomized into the tilt training and control groups. The home orthostatic self-training program consisted of daily sessions for 7 days a week for 4 weeks. In order to determine the effects of home orthostatic self-training, we repeated the head-up tilt test in both groups 4 weeks later. Among the tilt-training group, 9 of 16 patients (56%) had a positive response on follow-up head-up tilt test. Among the untreated control group, 9 of 17 patients (53%) had a positive response on follow-up head-up tilt test. In subgroup analyses according to the number of tilt-training sessions or the classified type, we found no differences in the follow-up head-up tilt test responses. Spontaneous syncope or presyncope over mean follow-up of 16.9 months were observed in 42.9% versus 47.1% in the tilt-training and control group, respectively. CONCLUSIONS: Home orthostatic self-training was ineffective in reducing the positive response rate of head-up tilt test in patients with recurrent neurally mediated syncope.     

The Use of Serotonin Reuptake Inhibitors for the Treatment of Recurrent Syncope Due to Carotid Sinus Hypersensitivity Unresponsive to Dual Chamber Cardiac Pacing

Carotid sinus hypersensitivity can be a cause of recurrent unexplained syncope in the older patient. Dual chamber cardiac pacing may relieve the bradycardia, but may not affect the vasodilatory component of this disorder. We report on two patients with carotid sinus hypersensitivity with a predominant vasodilatory component who experienced recurrent syncope following permanent pacemaker implantation. Both patients were treated with serotonin reuptake inhibitors and after 4–6 weeks of therapy had complete resolution of symptoms. We conclude that serotonin reuptake inhibitors may be useful in the treatment of recurrent syncope due to carotid sinus hypersensitivity resistant to dual chamber cardiac pacing.     

Carotid Sinus Hypersensitivity is Common in Patients Presenting with Hip Fracture and Unexplained Falls

Background: We tried to determine the prevalence of carotid sinus hypersensitivity (CSH) in patients with hip fractures with and without a clear history of an accidental fall.
Methods: We studied 51 patients hospitalized for a hip fracture and 51 matched controls from our outpatients department. All patients were subjected to a carotid sinus massage in the supine and upright position . Patients were categorized in accidental (Group A) and unexplained (Group B) fallers.
Results: Six of 33 (18.2%) patients in Group A and 12 of 18 (66.7%) patients in Group B ( P < 0.001) had a positive response to the carotid sinus massage. Nine controls (17.6%) also demonstrated CSH. Patients in Group B were older (A: 75.5 ± 8.5 years vs B: 80.1 ± 5.9 years, P = 0.029) and were more likely to have a history of unexplained falls or syncope in the past (A: 0% vs B: 66.7%, P < 0.0001) than individuals in group A. Vasodepressor/mixed forms accounted for the majority of CSH responses in Group B (75%). When compared with the control group, CSH was still more common in Group B (B: 66.7% vs control: 17.6%, P < 0.0001) but not in Group A (A: 18.2% vs control: 17.6%, P = 1.000).
Conclusions: The prevalence of CSH is increased in elderly patients with hip fractures, only in those who present with an unexplained fall and report a history of syncope or unexplained falls in the past. The vasodepressor/mixed forms account for the majority of CSH responses in the group of unexplained fallers.     

Clinical Experience with Thera DR Rate-Drop Response Pacing Algorithm in Carotid Sinus Syndrome and Vasovagal Syncope

This study examined the effectiveness of cardiac pacing using the Thera DR rate-drop response algorithm for prevention of recurrent symptoms in patients with carotid sinus syndrome (CSS) or vasovagal syncope. The algorithm comprises both diagnostic and treatment elements. The diagnostic element consists of a programmable "window" used to identify heart rate changes compatible with an evolving neurally mediated syncopal episode. The treatment arm consists of pacing at a selectable rate and for a programmable duration. Forty-three patients (mean age 53 ± 20.4 years) with CSS alone (n = 8), CSS in conjunction with vasovagal syncope (n = 4), or vasovagal syncope alone (n = 31) were included. Thirty-nine had recurrent syncope, while the remaining four reported multiple presyncopal events. Prior to pacing, 40 ± 152 syncopal episodes (range from 1 to approximately 1,000 syncopal events) over the preceding 56 ± 84.5 months. Postpacing follow-up duration was 204 ± 172 days. Three patients have been lost to follow-up and in one patient the algorithm was disabled. Among the remaining 39 individuals, 31 (80%) indicated absence or diminished frequency of symptoms, or less severe symptoms. Twenty-three patients (23/29, or 59%) were asymptomatic with respect to syncope or presyncope. Sixteen patients had symptom recurrences. Of these, seven experienced syncope (7/39, or 18%) and 9 (29%) had presyncope: the majority of patients with recurrences (6/7 syncope and 7/9 presyncope) were individuals with a history of vasovagal syncope. Consequently, although symptoms were observed during postpacing follow-up, they appeared to be of reduced frequency and severity. Thus, our findings suggest that a transient period of high rate pacing triggered by the Thera DR rate-drop response algorithm was beneficial in a large proportion of highly symptomatic patients with CSS or vasovagal syncope.     

Evaluation of Sinus and Atrioventricular Nodes Function in Patients with Vasovagal Syncope

Aim: Evaluation of sinus and atrioventricular nodes function as a potential factor responsible for prolonged bradycardia, asystole, or both in patients with cardioinhibitory and non-cardioinhibitory vasovagal syncope (VVS). The study included 258 patients (mean age = 47.7 ± 17.2 years; range 18–62; 147 females) with a history of VVS. They were divided among four groups, according to results of head-up tilt test (HUTT).
Methods: All patients underwent standard HUTT, carotid sinus massage (CSM), and rapid transesophageal atrial pacing for evaluation of total sinus node recovery time (SNRT), and corrected sinus node recovery time (CNRT), resting and intrinsic heart rate (IHR), and Wenckebach point (WP). Values of SNRT > 1,500 ms, CNRT > 525 ms, WP < 130 bpm, and CSM-induced pause >3 seconds were considered abnormal.
Results: SNRT, CNRT, and WP before and after pharmacological blockade, resting heart rate, and IHR did not differ significantly among the study groups. The prevalence of mild sinus node dysfunction (SND), decreased value of WP, and cardioinhibitory carotid sinus hypersensitivity was similar among all study groups.
Conclusions: The prevalence of mild SND, abnormal atrioventricular conduction, and carotid sinus hypersensitivity (CSH) was similar among patients with VVS regardless of the type of vasovagal reaction. SND and CSH do not seem to play an important role in the pathogenesis of cardioinhibitory vasovagal reaction.     

Sitcom syncope: a case series and literature review of gelastic (laughter-induced) syncope

Syncope is a common complaint that is frequently evaluated without identifying a precipitating cause. Gelastic (laughter-induced) syncope is an uncommon and poorly understood condition. We describe 3 patients who experienced loss of consciousness during vigorous laughter. Each patient had an extensive medical evaluation, including a comprehensive history and physical examination, 12-lead electrocardiography, chest radiograph, routine blood analysis, polysomnography, tilt table testing, 2-dimensional transthoracic echocardiography, nuclear or echocardiographic stress testing, and 24-hour Holter monitoring. All 3 patients had an abnormal response to head-up tilt table testing, with either a significant decrease in systolic blood pressure or inappropriate heart rate response on achieving an upright position. These observations together with our review of the literature suggest that gelastic syncope may be a variant of vasodepressor syncope. Knowledge of this condition, its pathophysiology, and potential treatment options may be of value to clinicians when evaluating patients with unexplained loss of consciousness.     

Carotid sinus hypersensitivity and syncope

The patient with a hypersensitive carotid sinus reflex and syncope may pose special challenges in evaluation and treatment. Specifically, although the finding of carotid sinus hypersensitivity may indeed indicate an exaggerated vagal tone that causes syncope, it may also be a chance association in a patient with syncope due to another cause. Careful clinical and electrophysiologic testing may be needed to distinguish these two possibilities. Furthermore, the need for drug therapy or cardiac pacing (or both) must be determined on an individual basis, depending on the relative contributions of cardioinhibitory and vasodepressor components to the patient's symptoms and also on the degree of patient limitation.     

Diagnosis and management of vasovagal syncope and dysautonomia

Vasovagal syncope is a condition better known as neurocardiogenic or neurally mediated syncope. Dysautonomic syncope is the irregular neuroautonomic response during the body's attempt to maintain homeostasis. Both types of syncope are associated with orthostatic hypotension and are nonlethal. The underlying pathophysiology manifests the vast symptoms suffered by the individual. Research continues to develop new markers to improve diagnostic testing and therapies for treatment. Advanced practice nurses now have a new tool with Head-Up Tilt Training Programs to offer the patients who suffer from frequent and refractory neurocardiogenic and dysautonomic syncope.