Syncope: The Ups and Downs
Authors:
Chad Kessler, MD, Section Chief, Emergency Medicine, Jesse Brown VA Medical Center, Clinical Associate Professor, Departments of Emergency Medicine and Medical Education, Associate Program Director, EM-IM Program, University of Illinois at Chicago School of Medicine.
Jenny Tristano, MD, EM-IM Program, University of Illinois at Chicago School of Medicine.
Peer Reviewer:
Jason Knight, MD, Emergency Medicine Department, Maricopa Medical Center, Phoenix, AZ.
Sandra M. Schneider, MD, Editor
Clinical Scenarios
Case 1. Lily is a 23-year-old female nursing student who presented after losing consciousness. Lily was watching an EM nurse clean a wound for eventual suturing. Lily complained of nausea and dizziness, then passed out and fell to the floor. The witnessing nurse called for help, but noticed that for approximately 30 seconds the patient was making jerking motions consistent with a possible seizure. Lily was taken to a bay in the emergency department, and IV fluids were started. After a few minutes, she began to wake up and answer questions appropriately. A blood glucose check was performed and was normal.
Case 2. Sarah is a 65-year-old female with a past medical history of hypertension, fibromyalgia, and depression, who presented with a complaint of feeling lightheaded. She reported that she was at work today, sitting at her desk performing data entry, when she started to feel her heart race and felt like she was going to pass out. Her symptoms lasted approximately two minutes, then resolved. The patient denied any loss of consciousness at the time. The patient reported feeling back to baseline when a similar episode occurred 30 minutes later. Her co-worker brought her to the emergency department for evaluation.
Case 3. Steve is a 75-year-old male with a past medical history significant for hypertension and high cholesterol, who presents after losing consciousness while walking. According to the patient's wife, they were on their usual daily walk around the neighborhood when the patient "passed out." The patient's wife was able to support her husband and lay him down on the ground, and she called 911. While waiting for the ambulance to arrive, the patient regained consciousness.
Introduction
Syncope is a common complaint in the emergency department (ED). Patients with syncope can present in different manners, have multiple associated causes, and have a range of outcomes. An extensive number of ancillary tests can be used to evaluate syncope, but the emergency physician has to balance the possibility of missing a potentially dangerous diagnosis against committing time, cost, and placing a patient at risk for serious side effects from unnecessary testing. In recent years, the evaluation of syncope in the ED has become primarily directed at risk-stratification — identification of patients at risk for a short-term adverse outcome — rather than a specific diagnosis. If the patient is identified as low-risk, inpatient observation and monitoring has no proven benefit, and further evaluation can be done as an outpatient. This article will provide an overview of the current evidence regarding the presentation and evaluation of syncope. It also strives to synthesize the information into a format that will be efficiently accessible to clinicians when making management decisions.
Background
Syncope is characterized by a sudden, transient loss of consciousness (T-LOC) associated with the inability to maintain postural tone. Recovery is spontaneous and occurs after a brief time period without intervention.1-2 There is no single prototypical syncopal episode. Loss of consciousness can occur differently from person to person, making it difficult to differentiate syncope during initial and even subsequent evaluations. In order to be classified as syncope, after loss of consciousness patients must regain complete baseline neurologic status spontaneously, promptly, and independently.3-8
Even though the definition of syncope seems specific, it is actually one of the biggest areas of disagreement among researchers.9 In 2010 a multicenter, observational study was carried out in 19 hospitals in a public health system. Data were prospectively collected through questionnaires that were completed for all patients who presented to the ED for T-LOC. As part of the study, EPs had to further classify patients as syncopal versus non-syncopal T-LOC. The study's steering committee also reviewed the data and made final diagnoses according to European Society of Cardiology (ESC) guidelines. The final analysis included 1419 patients, with 1217 classified as syncopal and 202 classified as non-syncopal T-LOC according to ESC guidelines. They found that EPs had correctly diagnosed syncope in 84% of patients. This showed a 16% discordance rate between the definition used in practice by EPs and that used by the ESC.10
Historically, "syncope" referred to T-LOC of cardiovascular origin as opposed to other causes of T-LOC. Later, syncope then became viewed as a particular syndrome on a broader spectrum of T-LOC presentations.1 More recently, researchers have referred to the two terms interchangeably, with many using "syncope" as a broad term to describe any presentation primarily characterized by a loss and regaining of consciousness, particularly those of unknown etiology.11-12
The issue is further complicated by syndromes with incomplete loss of consciousness, termed near-syncope or pre-syncope. The research in this area is limited, especially since in the majority of studies pre-syncope is an exclusion criterion. However, a small study by Grossman et al compared 30-day outcomes in those presenting with syncope to those presenting with near-syncope and found no significant difference in the number of adverse outcomes or critical interventions required by the two groups.13 These findings support an already common practice that near-syncope has the same morbidity and mortality as syncope and deserves the same workup.4 This study also showed that even though the morbidity and mortality was similar, pre-syncope patients were not admitted as often and did not received the same workup as syncope patients. In fact, only 49% of pre-syncope patients were admitted compared to 69% of patients with syncope.
Understanding the definition is more than semantics. Syncope accounts for 0.9% to 3% of ED visits and up to 6% of hospital admissions.14-16 As many as 60% of syncope patients are eventually admitted, depending on patient age and co-morbidities, with the majority of hospital admissions being non-diagnostic.8,15 Syncope hospitalizations cost anywhere from $1.7 to $2.4 billion annually.17-18 High admission rates exist because of the serious morbidity and mortality that occurs in up to 6% of patients after presentation to the ED. For high-risk syncope, especially cardiovascular syncope, this morbidity and mortality rate increases to up to 30%.14-15 Up to 0.7% of patients with syncope will die within 7-30 days after presentation, and 6-14% will die within the next year.19-24 Of all serious outcomes that will happen after ED presentation, 48% will occur within the first month, but the remainder will continue in a steady and significant pace throughout the following year.20
Pathophysiology
An overview of possible syncope etiologies can help guide investigation. The common process that leads to syncope is a transient decrease in blood flow that reduces cerebral perfusion and leads to a transient loss of consciousness.25-26 However, there are multiple mechanisms by which this can occur. Many authors have provided multiple ways of classifying the different etiologies of syncope. The reality is that syncope is very difficult to classify because of the significant amount of physiologic overlap involved in various presentations. The one common theme is a division between those causes that are and are not primarily cardiac in origin.11-12 (See Table 1.)
Table 1: Classification of Syncope*1,2,4,11,25
Cardiac/Cardiovascular |
Reflex (Neurocardiovascular) |
Non-cardiovascular |
* This list is not exhaustive |
||
Arrhythmias
Structural Abnormalities
Hemodynamic Compromise
|
Situational
Vasovagal
Carotid Sinus Sensitivity/Syndrome Autonomic Failure
|
Neurologic
Toxic/Metabolic
Psychogenic |
Included in cardiac syncope are arrhythmias, structural lesions, and hemodynamic compromise. In arrhythmias, the electrical system of the heart impairs the heart's ability to generate continuous adequate blood flow. Structural lesions tend to be obstructive and prevent forward flow. Hemodynamic compromise, such as might come from hypovolemia secondary to blood loss or relative hypovolemia from cardiac tamponade, impairs the heart's ability to fill with the blood it needs to pump.1
Improper functioning of the neural mechanisms that are normally responsible for controlling the circulation contributes to reflex or neurocardiogenic syncope. In vasovagal or situational syncope, these same neural mechanisms become overactive. Previously well-documented triggers include "neck tie" syncope, micturation syncope, and cough-triggered syncope, as well as many others. A trigger causes a sudden drop in systolic blood pressure, often accompanied by a sudden, paradoxical decrease in heart rate.27 With carotid sinus hypersensitivity, the carotid sinus is over-stimulated, which leads to an extended pause in heart beat and a drop in blood pressure seen by the brain. In autonomic failure, there is impairment of function and failure of the normal mechanisms that maintain perfusion. This is usually the result of another primary disease process.
Non-cardiovascular syncope encompasses causes that are unrelated to a primary cardiovascular process and often is referred to as "pretenders" or syncope mimics. These include neurologic insults such as seizures, transient ischemic attacks, stroke, metabolic insults, and psychogenic syncope. These conditions are not primarily cardiovascular, but they can cause a similar clinical presentation as cardiogenic syncope.
Syncope Evaluation
History. The history and physical exam plus electrocardiogram (ECG) are the most important parts of the syncope workup.4,11,28-29 The history, physical exam, and ECG alone can arrive at the diagnosis in more than 50% of ED cases.30 The details of the episode help guide evaluation. The first step is to identify a syncopal or a pre-syncopal episode. Patients will not always report "passing out" or a "black out." They may more vaguely describe a situation. They might present with trauma from a fall but may not necessarily remember the events of the fall or what caused the fall. It is important to determine if the patient passed out, got dizzy and then fell, or just had a mechanical fall. With pre-syncope, patients may complain of "dizziness," "lightheadedness," "being woozy," or feeling "unsteady."4,30-31 Once identified, a physician should help the patient and any witnesses clearly retrace the events leading to the episode. (See Table 2.) It can be helpful to approach the interview chronologically.
Table 2: The Interview and the Episode
Prior to Episode (often obtained from patient): During Episode (often obtained from witnesses): After Episode (often obtained from witnesses): |
There are a few situations in which a history can also be confounding or misleading. Caution should especially be exercised in older adults because they are less likely to report the typical symptoms normally associated with a particular diagnosis.32 Syncope can sometimes be difficult to distinguish from a seizure because a patient can experience myoclonic jerks during syncope that a layperson may mistake for a seizure. Especially when presenting with a first-time seizure, it is important to ask details about the episode before concluding the episode was a seizure. Were the patient's eyes open? Was there incontinence or tongue biting? Did the patient have a prolonged duration of confusion after the episode?
After obtaining a description of events, there should be a focus on the patient's past medical history.33-34 Patients should be asked about a history of coronary artery disease, valvular disease, cardiomyopathies, arrhythmias, as well as about risk factors for cerebrovascular accidents (CVA) and clotting disorders. This history must also include the medications the patient is actively taking and recent changes to their medication regimen. The older the patient, the more likely that polypharmacy is a potential cause. One should also inquire if the patient has had any previous similar events, as previous syncopal episodes place patients at an increased risk for recurrence. There should also be a focus on family history, including syncopal episodes, cardiac disease, arrhythmias, or sudden death in relatives.
Clinical Scenarios
Case 1. After Lily woke up, she was almost immediately available to give more information about her history. She admitted that this was her first experience with a significant amount of blood. She also reported that she had not had anything to eat that morning because she was running late for her clinical. She denied any chest pain before the episode, and only confirmed feeling nausea and dizziness, with no other symptoms. She denied any previous personal history of passing out. She did not report any significant medical problems on review of systems, including no history of seizures or diabetes. Her only medication was an oral contraceptive pill she had been on for several years without any recent change. She denied any family history of heart disease.
Case 2. Sarah was unable to provide an additional description of her symptoms. She did note that she had experienced similar episodes previously for short amounts of time, but had always thought they were related to anxiety because they went away after a few seconds. This was the first time she had thought she might lose consciousness. She reported she was currently taking tramadol for pain, hydrochlorothiazide for blood pressure control, and citalopram as her regular medications. There had been no recent change, but her doctor had told her that he was thinking of starting her on another medication for blood pressure control. Her family history included two living parents with hypertension, but no known history of sudden cardiac death in any family members.
Case 3. Steve was unable to describe any additional symptoms prior to his episode. While this was the first time he had ever lost consciousness, he did admit that for the past five weeks his daily walks with his wife had been making him tired. He had considered himself physically fit for his age, but had noticed that the same distance he used to walk made him feel "weak." The patient reported he was currently taking lisinopril for blood pressure control and losartan for his cholesterol. He reported both of his conditions were considered well-controlled by his physician. He reported both of his parents had lived into their late 90s and died of old age.
Physical Exam
While the history can help guide special physical exam maneuvers, there are some parts of the exam that should always be performed.29,34 First, a complete set of vital signs should be obtained, looking for tachycardia, bradycardia, hypotension, and hypoxia. Included should be a set of orthostatic vital signs, as these can frequently be helpful. Cardiac auscultation should look for murmurs that may indicate an obstruction or a friction rub, which may point to pericarditis. In a younger patient, such as an athlete with syncope after exertion, valsalva should be performed to listen for an increase in intensity of a systolic murmur, which could indicate hypertrophic obstructive cardiomyopathy. One should look for jugular venous distension and/or pulsus paradoxus in patients who present with shortness of breath, tachycardia, and/or hypotension. JVD may indicate CHF as a potential cause.
Carotid sinus massage can help evaluate carotid sinus sensitivity. If the maneuver leads to a ventricular pause lasting more than three seconds and/or a fall in systolic BP of greater than 50 mmHg, this can be diagnostic.1 However, this maneuver is contraindicated in patients with report of TIA or stroke in the past three months or in patients with a carotid bruit. Most textbooks and articles suggest that carotid massage should also not be performed in patients older than the age of 65 years due to the risk of carotid artery disease, carotid plaques, and stroke.
Depending on the events surrounding the episode, for example if there was a fall, motor vehicle collision, or some other potential trauma experienced as a result of loss of consciousness, a complete head-to-toe examination should be performed to look for secondary injuries that may need evaluation. This is also a good time to look for oral lesions such as those from tongue biting and for evidence of incontinence that may point to a seizure. A thorough neurologic exam should be performed to look for evidence of a stroke. A rectal exam is indicated if a GI bleed is suspected as a cause of syncope.35 GI bleeds should be especially suspected in the setting of older patients who present with tachycardia or hypotension, or in anyone with a past history of gastrointestinal bleeding or malignancy.
Clinical Scenarios
Case 1. On physical exam, Lily's vital signs were unremarkable. She had a normal blood pressure and heart rate. Orthostatic vital signs were taken and did not show any significant changes in blood pressure or heart rate with positional change. She had no murmurs on cardiac auscultation. She was noted to have a 2 cm laceration in the middle of her forehead that she had sustained from the fall. A cervical collar was placed to protect her C-spine, given the head trauma. The remainder of her neurologic exam was normal.
Case 2. On physical exam, Sarah's blood pressure was elevated to 170/92 and her heart rate was regular at 73 bpm. The rest of her vital signs were normal. Her physical exam was notable for the patient being overweight, and the cardiac exam was limited secondary to body habitus. The neurologic exam was normal, including normal cerebellar function. The remainder of the physical exam was also normal.
Case 3. On physical exam, Steve's vital signs were all within normal limits. The physical exam was most notable for a holosystolic murmur that softened toward the end of systole. The remainder of his physical exam was otherwise normal.
Ancillary Tests
Most evidence has shown that additional testing should be guided by the patient's presentation. However, there are certain tests that have become standard.26 The ECG is an affordable, cost-effective screening exam that should be performed on all syncope patients.31 It is one of the few interventions that has been well-studied, and on its own can be responsible for diagnosing anywhere from 1% to 11% of syncope patients.36-38 Patients should also be concurrently placed on a cardiac monitor during their ED evaluation, as any abnormality on an ECG or rhythm strip can indicate increased patient risk.39
Some ECG patterns are associated with increased risk of serious arrhythmias and sudden cardiac death.40 Bradycardia, tachyarrhythmias, AV nodal block, and bundle-branch blocks suggest the potential for decreased cardiac output resulting in inadequate cerebral perfusion during times of increased cardiovascular demand that results in syncope. Also, abnormal electrical activity seen on the ECG in asymptomatic patients correlates with the development of symptomatic and potentially serious tachyarrhythmias, including pre-excitation syndromes (e.g., Wolff-Parkinson-White syndrome with short PR interval and delta waves seen during the initial QRS complex), Brugada syndrome (right bundle-branch block with ST-segment elevation in V1 to V3), long QT syndrome (QTc interval > 470 msec in men and > 480 msec in women), and arrhythmogenic right ventricular dysplasia (QRS duration > 110 msec in leads V1 to V3 with inverted T waves). However, as in all ECG considerations, it is important to interpret the clinical relevance of the ECG pattern according to the clinical circumstances. For example, an isolated prolonged QT interval does not necessarily indicate the patient is at risk for sudden death.
A bedside blood glucose test can also be immediately helpful. There is limited evidence supporting other tests, but a urine pregnancy, complete blood count, and serum chemistries are quite common.3,7 Other common tests to consider on a case-by-case basis depending on the presentation include a blood alcohol level, urine toxicology screen, and cardiac biomarkers.41 D-dimer is also occasionally ordered, as pulmonary embolism is a well-documented potential etiology of syncope. Recent studies have investigated the utility of creatine kinase levels to differentiate syncope from potential seizure and BNP levels as a prognostic indicator for cardiac syncope, but there are insufficient data currently to make these a standard part of practice.35,42
A chest X-ray is also a common order. A CT scan of the brain tends to be reserved for older patients or those presenting with new or focal neurologic symptoms. A head CT should also be considered in patients with head trauma after a syncopal episode and in patients on anti-coagulants. A CT scan of the head in uncomplicated or isolated syncope is usually low yield.
An echocardiogram, carotid duplex ultrasound, and electrophysiologic studies such as tilt-table testing can be diagnostically helpful, but these are usually performed on an inpatient basis and are not a part of the standard ED evaluation.43
Clinical Scenarios
Case 1. Lily had an electrocardiogram performed, which showed normal sinus rhythm, and had a negative urine pregnancy test. CT scans of the head and the cervical spine showed no acute or abnormal findings. No further evaluation was performed.
Case 2. Sarah's ECG showed a normal sinus rhythm, which barely met the criteria for left ventricular hypertrophy, but showed no arrhythmia or evidence of an acute coronary syndrome. A chest X-ray showed a slightly enlarged cardiac silhouette, but was unchanged compared with previous X-rays on file. A complete blood count, basic metabolic profile, and troponin level were all within normal limits.
Case 3. Steve had an ECG that showed a normal sinus rhythm without any abnormal morphology. A chest X-ray showed no significant abnormalities. A complete blood count, basic metabolic profile, and troponin level were all sent. The blood count was notable for hemoglobin of 8.5 g/dL. On repeat questioning, the patient denied any recent trauma, weight loss, hematochezia, or other abnormalities. A rectal exam was performed and a bedside hemoccult was positive.
Disposition
Even after careful assessment, up to 50% of syncope patients do not have a diagnosis after ED evaluation.36,44 The issue for the EP becomes how to disposition these patients. Multiple risk-stratification tools have been developed with the goal of sufficient sensitivity to capture and recommend admission for all patients with potentially serious etiologies while avoiding further inpatient workup for patients most likely to have benign etiologies. (See Table 3.)
Table 3: Commonalities of Syncope Risk Stratification Rules45
Risk Stratification of Patients with Syncope |
OESIL Risk Score(Colivicchi et al23)* |
Derivation of the San Francisco Syncope Rule |
Boston Syncope Criteria (Grossman et al47) |
EGSYS scoring system (Del Rosso et al48) |
*Increasing number of risk factors indicates increased risk of mortality. |
||||
Abnormal ECG |
Abnormal ECG |
Congestive heart failure history |
Signs and symptoms of acute coronary syndrome |
Palpitations preceding syncope |
Age > 45 years |
Age > 65 years |
Hematocrit < 30% |
Signs of conduction disease |
Heart disease and/or abnormal ECG |
History of ventricular arrhythmia |
Cardiovascular disease in clinical history |
Abnormal ECG** |
Worrisome cardiac history |
Syncope during effort |
History of CHF |
Syncope without prodrome |
Shortness of breath |
Valvular heart disease by history or by physical exam |
Syncope while supine |
Systolic blood pressure < 90 mm Hg at triage |
Family history of sudden death |
Presence of precipitating and/or predisposing factors (Points: -1) |
||
Persistent abnormal vital signs in the ED |
Presence of autonomic prodromes |
|||
Volume depletion such as persistent dehydration, GI bleeding, or hematocrit < 30 |
||||
Primary CNS event |
||||
Unfortunately, while some of these rules have shown high sensitivity in their derivation and validation phases, none have produced 100% sensitivity with external validation.49 (See Table 4.) When the sensitivities are very high, they tend to recommend a high concurrent rate of admission that in the end saves little in terms of resources. A recent pooled meta-analysis was performed of all studies available to date regarding clinical decision rules for evaluation of syncope in the ED.50 It showed that none of the rules has sufficient sensitivity to be relied upon entirely or enough specificity to really make an impact on admissions. Currently, clinical decision rules can serve as evidence to help support a clinician's decision or to contribute to the thought process. Given that many of the clinical decision rules have overlapping criteria, a suggested pathway for considering these guides in the context of a patient is presented. (See Table 5.) In the end, though, the clinical decision rules should never be the sole basis on which a decision is made.19,51-53
Table 4: Sensitivities and Specificities of Various Risk Stratification Systems for Syncope45
Study |
System |
Derivation Sensitivity |
Derivation Specificity |
Validation Sensitivity |
Validation Specificity |
Quinn et al 2004 |
Derivation SFSR |
96.2% (95% CI 92% to 100%) |
61.9% (95% CI 58% to 66%) |
— |
— |
Quinn et al 2005 |
Physician Judgment |
94% (95% CI 86-94%) |
52% (95% CI 51-53%) |
— |
— |
Quinn et al 2006 |
Validation SFSR |
— |
— |
98% (95% CI: 89 to 100%) |
56% (95% CI 52 to 60%) |
Sun et al |
External Validation SFSR All 7 day outcomes |
— |
— |
89% (95% CI 81-97) |
42% (95% CI 37-48%) |
— |
External Validation SFSR Delayed 7 day outcomes |
— |
— |
69% (95% CI 46-92%) |
42% (95% CI 37-48%) |
Birnbaum et al |
Failure to Validate SFSR |
— |
— |
74% (95% CI 61% to 84%) |
57% (95% CI 53% to 61%) |
Schladenhaufen et al |
Application SFSR in Elderly ED Patients |
— |
— |
76.5% (95% CI 66.7% to 84.3%) |
36.8% (95% CI 32.2% to 41.6%) |
Reed et al |
ROSE pilot High Risk only |
0.636 (p value 0.035) |
0.716 (p value 0.035) |
— |
— |
Reed et al |
ROSE pilot High/Med Risk |
1.000 (p value 0.203) |
0.182 (p value 0.203) |
— |
— |
Grossman et al |
Boston Syncope Criteria |
— |
— |
97% (95% CI 93-100%) |
62% (95% CI 56-69%). |
Del Rosso et al |
EGSYS |
95% (CI 84.4-99.4) |
61% (CI 54.3 to 76.6%) |
92% (CI 76.9-98.2) |
69% (CI 62.7-75.2) |
The other issue is that there is no consensus yet on how long after syncope presentation in the ED patients should be monitored for adverse outcomes. Studies have followed patients for various durations, looking at both short-term outcomes from 7 to 30 days and long-term outcomes for up to a year. Adverse events occur at increased rates for syncope patients in both time frames. Prediction is more complicated by evidence that shows factors that predict short-term serious outcomes are different from those factors that predict longer-term serious outcomes.20,55-57
A recent study looked at risk factors for mortality and rehospitalization for syncope at up to 27 months after initial presentation. Medical records were reviewed for 325 patients; at 27 months, 4% were rehospitalized for syncope and 12% had died. Significant independent prognostic factors for rehospitalization for syncope were: history of diabetes (odds ratio [OR] 5.7, 95% confidence interval [CI] 1.6-20.4), history of atrial fibrillation (OR 4.0, CI 1.0-15.6), and smoking (OR 4.6, CI 1.3-16.8). Significant independent prognostic factors for time to mortality were history of diabetes (hazard ratio [HR] 2.7, CI 1.4-5.2), history of coronary artery bypass graft surgery (HR 2.9, CI 1.3-6.5), history of malignancy (HR 2.5, CI 1.2-5.2), narcotics use (HR 4.0, CI 1.7 to 9.8), smoking (HR 2.8,CI 1.4-5.5), history of atrial fibrillation (HR 2.4, CI 1.0 to 5.4), and volume depletion (HR 2.8, CI 1.4-5.8). This study also calculated the risk scores of two well-known decision rules, the San Francisco Syncope Rule (SFSR) and the OESIL risk score. Neither score was able to predict long-term mortality or rehospitalization.58
Aside from clinical prediction rules, there are some smaller studies that have attempted to find laboratory tests whose values might correlate with increased morbidity and mortality risk after syncope.59 Abnormal BNP concentration and troponin values are possible predictors of adverse outcomes; however, there is insufficient evidence to recommend obtaining these tests as a part of a standard ED evaluation in all patients. For now, they should be ordered within the appropriateness of the clinical context.
Clinical Scenarios
Case 1. Lily's cervical spine was cleared, her C-collar was removed, and her laceration repaired. Given the circumstances of the episode, including her rapid return to baseline mental status with no post-ictal, her lack of medical history, normal physical exam, and normal ancillary test results, Lily was diagnosed with vasovagal syncope and discharged to follow up with her primary physician for suture removal. She was also counseled that in the future, she should sit while watching new medical procedures until she becomes more acclimated.
Case 2. Sarah's evaluation did not yield a dangerous cause for what were classified as pre-syncopal episodes. Her ECG did show evidence of ventricular hypertrophy. When this was considered with the patient's age and history of poorly controlled hypertension, the patient was admitted to the telemetry floor for observation and further evaluation. While on telemetry overnight, the patient once again had an episode of palpitations. Her telemetry showed atrial fibrillation with rapid ventricular response that lasted for approximately three minutes and self-converted back to normal sinus rhythm. During her inpatient stay, Sarah underwent evaluation for her atrial fibrillation and was treated appropriately.
Case 3. Steve's age, heart murmur on physical exam, and low hemoglobin led to an inpatient evaluation. An echocardiogram showed evidence of aortic stenosis with a valve area of 1.2 cm2. A colonoscopy showed an angiodysplastic lesion, which was treated endoscopically. The patient was transfused to a hemoglobin level of 10 g/dL and exercised around the hospital floor with improvement in fatigue and no recurrent syncopal episodes. He was discharged home to follow up with cardiology and cardiovascular surgery to monitor symptoms and plan for eventual aortic valve replacement.
Future Directions
Currently there are several different strategies being evaluated for their efficiency and efficacy in the evaluation and management of syncope. These include syncope-specific observation wards, some of which are already in operation, to speed patients through specific evaluation protocols.60 There are also syncope-specific clinics and evaluation centers. There is still work on deriving a clinical decision rule that balances sensitivity and specificity. Another approach being developed is standardizing the workup of syncope after presentation, relying on an algorithm and systemization to increase efficiency to diagnosis and decrease unnecessary tests.61-62 Like most areas of medicine, the solution for managing syncope will likely be a blending of multiple methods.
Conclusion
Syncope is one of the most frequent complaints emergency physicians encounter. Additionally, its incidence is high regardless of practice setting. The emergency physician should be on alert because a patient's reported chief complaint may be masking a more subtle presentation of syncope that carries a significant risk of morbidity and mortality. Likewise, pre-syncope and syncope should be evaluated similarly. Determining the cause of an episode is complicated by the various physiology pathways that all lead to a similar scenario at presentation. The vital pieces of the evaluation are the history, physical exam, and ECG. All other ancillary testing should be guided by the context surrounding the patient's presentation. Most importantly, there is a lack of formal guidelines or decision rules that have demonstrated enough sensitivity to override clinician judgment. Attention to physical exam abnormalities, personal and familial cardiac risk factors, and the increased risk associated with patient age can help the clinician make thoughtful and safe disposition decisions.
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