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Europace : European pacing, arrhythmias, and cardiac electrophysiology, ISSN 1099-5129, 2013, Volume 15, Issue 10, pp. 1389 - 1406
Journal Article
European Heart Journal, ISSN 0195-668X, 10/2010, Volume 31, Issue 19, pp. 2369 - 2429
Rhythm control | CARDIAC & CARDIOVASCULAR SYSTEMS | Atrial fibrillation | LONG-TERM SURVIVAL | Anticoagulation | II RECEPTOR BLOCKADE | Upstream therapy | RADIOFREQUENCY CATHETER ABLATION | ANGIOTENSIN-CONVERTING ENZYME | Guidelines | Rate control | ANTIARRHYTHMIC-DRUG THERAPY | PARKINSON-WHITE-SYNDROME | European Society of Cardiology | Left atrial ablation | CARDIAC RESYNCHRONIZATION THERAPY | PULMONARY-VEIN ISOLATION | POLYUNSATURATED FATTY-ACIDS | CONGESTIVE-HEART-FAILURE | Pulmonary vein isolation | Recurrence | Postoperative Complications - etiology | Humans | Middle Aged | Secondary Prevention | Acute Coronary Syndrome - complications | Heart Valve Diseases - complications | Fibrinolytic Agents - therapeutic use | Electrocardiography | Adult | Atrial Fibrillation - diagnosis | Platelet Aggregation Inhibitors - therapeutic use | Heart Failure - etiology | Electric Countershock - methods | Precision Medicine | Sports | Primary Prevention | Stroke - prevention & control | Risk Assessment | Angioplasty, Balloon, Coronary - methods | Atrial Fibrillation - therapy | Ventricular Dysfunction, Left - etiology | Postoperative Complications - therapy | Thromboembolism - etiology | Anti-Arrhythmia Agents - therapeutic use | Mineralocorticoid Receptor Antagonists - therapeutic use | Catheter Ablation - methods | International Normalized Ratio | Point-of-Care Systems | Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use | Intraoperative Care | Atrial Fibrillation - etiology | Quality of Life | Acute Coronary Syndrome - therapy | Aged | Hemorrhage - chemically induced
Journal Article
Journal Article
Journal Article
by AUTHOR and Frank J Edwards and PEER REVIEWER and Steven M Winogra and Syncope can be divided into reflex (neurally mediated) syncope, hypotensive syncope, and cardiovascular syncope Presyncope is less serious, but in general should be evaluated like syncope Reflex syncope has three major causes: vasovagal, carotid sinus, and situational Cardiac syncope can be from abnormal rhythms or structural heart disease The electrocardiogram (ECG) may show some abnormalities, although the critical rhythm may have normalized All patients with syncope should have an ECG to assess for abnormal rhythm and Brugada ------------ Vasovagal Events and Carotid Sinus Syncope and Situational Syncope and Micturition Defecation Swallowing Coughing Laughing Hair grooming Fainting lark Many of the underlying mechanisms for situational reflex syncope syndromes are known, and include afferent triggers in the pulmonary, gastrointestinal, and genitourinary systems that provoke reflex vasodilation and bradycardia34 The main problem in making the diagnosis of situational syncope is failing to consider other potential causes It is important to perform a careful history and exam, and consider the presence of other risk factors, the patient’s age, and whether there is a history of similar events The “fainting lark” can be categorized as a form of situational syncope, although the mechanism is not pathologic per se This is a self-induced event, sometimes engaged in by adolescents and young adults for various reasons (including entertainment and malingering), wherein the individual squats, hyperventilates, then stands up abruptly while doing a Valsalva maneuver35 Syncope will follow in a majority of human beings through a combination of hypocarbia-induced peripheral vasodilation and cerebral vasoconstriction, along with the effects of suddenly standing while impeding venous return and increasing vagal output It has been used in a research setting to study blood pressure levels and other factors during syncopal episodes36 Orthostatic (Postural) Syncope After reflex syncope, the second leading cause of fainting is orthostatic or postural syncope, accounting for about 15% of fainting cases seen in the ED13 The normal human physiologic response to gravitational stress caused by rising from a lying or sitting position to an upright posture involves a complex autonomic compensatory response that keeps cardiac output and cerebral perfusion within narrow parameters An inadequate compensatory response for any number of reasons allows cerebral blood flow to fall A perfusion decrease of approximately 50% will initiate presyncope and may lead to an outright syncopal event13,34,37,38 In general, the orthostatic drop in pressure occurs within several minutes of the patient assuming a standing position, but significantly longer delays are possible More of an issue in older patients, orthostatic syncope can be divided into four categories: iatrogenic (ie, medication-related), volume depletion, primary autonomic dysfunction, and secondary autonomic dysfunction13,34 (See Table 1) Medication-induced failure of postural compensation is the most common cause of orthostatic syncope The list of drugs involved in inducing syncope by this mechanism is long and includes those drugs that interfere with autonomic cardiovascular reflexes, such as the beta-blockers, calcium channel blockers, alpha-blocking agents, and phenothiazines13 (See Table 3) By inducing fluid and electrolyte loss, diuretic agents cross over into the second category — volume depletion Volume depletion orthostatic syncope also is seen in patients experiencing dehydration or hemorrhage The third category of orthostatic hypotension falls under the rubric of primary autonomic nervous system failure A constellation of different diseases can lead directly to deterioration of autonomic pathways Examples include parkinsonism, Lewy body dementia, multiple-system atrophy (the Shy-Drager syndrome), and pure autonomic failure (PAF) Patients with these conditions exhibit an inability to maintain adequate cerebral perfusion when upright and even may have supine hypotension13 The final class of orthostatic intolerance is secondary autonomic failure, which refers to the autonomic neuropathies accompanying conditions such as diabetes, amyloidosis, familial dysautonomia, immune-related neuropathy, autoimmune autonomic ganglioneuropathy, Sjögren’s syndrome, paraneoplastic syndromes, and HIV neuropathy Diabetes is the most common pathology34 Angiotensin-converting enzyme inhibitors Alpha receptor blockers Calcium channel blockers Beta-blockers Phenothiazines Tricyclics Alcohol Opioids Diuretics Hydralazine Nitrates Sildenafil Monoamine oxidase inhibitors Two additional entities fall under the heading of postural orthostasis These are postprandial hypotension and postural orthostatic tachycardia syndrome (POTS) Studies show that nearly all nursing home patients experience some degree of postural hypotension after meals, especially following breakfast This is usually asymptomatic, but is related to some fainting episodes and falls with injury39 The risk of postprandial hypotension is higher in patients with multiple comorbidities POTS, on the other hand, is seen mainly in young patients and has been associated with syncopal episodes40 Mainly affecting post-pubertal females younger than 19 years of age, POTS consists of an increase in heart rate of 30-40 or more beats per minute on standing, accompanied by lightheadedness and weakness26 A diagnosis of exclusion, POTS may develop insidiously following an infectious disease such as mononucleosis Although it can become debilitating, the condition often resolves over a period of months with supportive treatment and conditioning40 Unless accompanied by syncopal symptoms, orthostatic blood pressure drops discovered during the ED evaluation of patients who present with presyncope or syncope must be interpreted with caution Many elderly individuals have asymptomatic baseline orthostatic changes41 Additionally, patients on autonomic response-blunting medications have significant comorbidities, such as coronary artery disease, hypertension, and diabetes, which put them at greater risk of cardiac-related syncope Therefore, orthostatic syncope is a diagnosis of exclusion when other etiologies have been evaluated to the extent warranted by age, history, and other clinical factors Cardiac Syncope Approximately 15% of syncope cases are due to cardiac causes, with two-thirds arising from arrhythmias and one-third related to cardiac structural disorders, both of which can lead to periods of inadequate cardiac output and diminished cerebral perfusion (See Table 1) Unlike patients with neurally mediated reflex syncope, who were shown in the Framingham Study to have no greater risk of death compared to a general population cohort, individuals with cardiac syncope were twice as likely to die of any cause during the Framingham Study’s 17-year duration42 Other studies show that the six-month mortality rate for patients with proven cardiac syncope is 10% or greater41 Concern that the event may be cardiac drives the high admission rates for older adults The list of arrhythmias associated with syncope includes any condition leading to slow, rapid, or disorganized rhythms41 (See Table 4) The first step in evaluating all syncope patients is to obtain an ECG Approximately 5% of older adults with syncope will have cardiac syncope diagnosed on the initial ECG, with such entities as supraventricular tachycardia, profound bradycardia, third-degree heart block, sick sinus syndrome, long sinus pauses (> 3 seconds), Mobitz type II atrioventricular (AV) block, and ventricular tachycardia43 Most often, the offending arrhythmia is no longer apparent and the ECG can be completely unremarkable In a prospective, multicenter, observational study, researchers identified more than 3,000 older adults (> 60 years) presenting with syncope (excluding those who had obvious cardiac syncope) and discovered that approximately 3% were diagnosed with a serious cardiac arrhythmia within the next 30 days The following initial ECG abnormalities predicted a two- to three-fold greater risk: nonsinus rhythm, multiple premature ventricular contractions, short PR interval, first-degree AV block, complete left bundle branch block, and Q wave/T wave/ST segment changes consistent with acute or chronic ischemia ECG abnormalities such as these are useful risk-stratification aids but are neither sensitive nor specific enough to determine the risk of a serious arrhythmic event43 (See Table 5) Bradycardia Sick sinus syndrome Second- or third-degree heart block Long and short QT syndrome Brugada syndrome Ventricular tachycardia Supraventricular tachycardia Pre-excitation pathway syndromes Atrial fibrillation and flutter Torsade de pointes Pacemaker malfunction Onset during exertion History of cardiac disease Electrocardiogram changes Lack of prodrome Palpitations at onset Chest pain Occurrence while supine Age > 60 years Family history of sudden death Other ECG abnormalities suggest a higher risk, including the genetically transmitted channelopathies such as the long QT syndrome (QTc > 450 ms for males, > 470 ms for females), short QT syndrome (QTc < 370 ms),44 and the delta wave and short PR interval of Wolff-Parkinson-White pre-excitation syndrome, a form of which is inherited Syncope patients always should be questioned about the presence of fainting spells or sudden death in family members Brugada syndrome is a rare hereditable mutation of a gene involved in the expression of myocardial sodium channels and is a well-recognized cause of sudden arrhythmic death45 The classic Brugada ECG demonstrates a pattern resembling right bundle branch block in leads V1-V3, with cove-shaped ST elevation with a J-point elevation of 2 mm or greater and T-wave inversion These classic changes may be expressed fully only when the patient receives a provocation dose of an agent such as the antiarrhythmic drug ajmaline Structural heart disease causes syncope by interfering with cardiac output when demand rises Exertional syncope in the elderly that is accompanied by chest pain and dyspnea is a classic presentation of critical aortic stenosis41 The most common etiology of sudden death in the younger age group is hypertrophic cardiomyopathy, which also predisposes patients to tachyarrhythmia events46 Fainting during exercise in otherwise healthy adolescents and young adults warrants concern for this inherited condition Other structural etiologies for syncope include myocardial ischemia, pericardial effusion, various cardiomyopathies, and atrial myxoma34,47 Infectious myocarditis can lead to syncopal events caused by structural myocardial dysfunction or by predisposing patients to tachyarrhythmias48 Pulmonary embolism (PE) can cause a form of structural syncope by interfering with pulmonary venous return and via other mechanisms In a recent multicenter Italian study, researchers evaluated patients admitted with a first syncopal episode and found an unexpectedly high prevalence (173%) of PE Researchers noted that PEs were discovered at a higher rate in patients who did not have alternative explanations for the syncopal event, but also in patients who did have alternative explanations49 The ED evaluation of syncope patients needs to include an assessment of PE risk factors along with attention to relevant vital sign abnormalities, such as tachypnea, sinus tachycardia, and hypoxia, and examination for signs of deep vein thrombosis Cardiac syncope is more likely in males older than 60 years of age who experienced no prodrome, and when the event occurs during exertion11 Another red flag is the presence of palpitations before the event Consider cardiac syncope when the faint happened while the patient was supine Syncope in Children Pediatric patients have fewer comorbidities and a more dynamic autonomic response than older adults Therefore, it is not surprising that approximately three-quarters of children and adolescents who presented to hospitals with syncope in one multicenter series were diagnosed with benign neurally mediated reflex syncope, and less than 3% were found to have cardiac-related syncope40,50 Up to half of all adolescent females and a quarter of adolescent males experience a vasovagal faint In otherwise healthy children from 6 months to 4 years of age, breath-holding spells can trigger a syncopal event The typical breath-holding spell (which may be seen in up to 5% of children) involves a triggering event such as a fall or being disciplined, after which the child cries, then holds his or her breath until facial cyanosis is visible and the child briefly loses consciousness, terrifying his or her caregivers51 At minimum, pediatric patients with syncope should receive an ECG The history should include the presence or absence of triggering events, prodromal symptoms, or palpitations Although vasovagal episodes after exertion are common, fainting during exercise is always concerning, as is a positive family history of early sudden death or suspicious syncope The presence of injuries suggests the fainting event occurred without warning Abnormal cardiac findings, including murmurs or signs or congestive failure, suggest a more serious cause Such findings warrant cardiology evaluation in a timeframe appropriate to the degree of concern Psychogenic pseudosyncope (PPS) events were observed at a rate of 23% in one large study of syncope in children and adolescents50 Patients with PPS may have a concomitant anxiety disorder or underlying depression PPS is classified as a conversion disorder and is seen most often in young females Possible clues include a history of frequent episodes with falls that do not lead to injury, and episodes of unresponsiveness that last longer than the typical syncope duration of a minute or less52 Syncope in Athletes Most syncopal events in athletes are neurally mediated reflex events53 However, even a benign syncopal event that occurs during the performance of technically dangerous athletic activity, such as motor sports or diving, raises the risk of serious injury In one large series of athletes undergoing screening evaluations, 12% reported an episode of post-exertional syncope during the past five years A smaller percentage experienced fainting during exercise, and in this group, there was a higher frequency of cardiac causes Important items in the history may include a prodrome, palpitations, medication use, family history of sudden death at an early age, and an event occurring during actual exertion Athletes who experience syncope during exertion require a focused cardiology evaluation searching for the presence of such entities as hypertrophic cardiomyopathy, ion channel disorders, and right ventricular outflow tract arrhythmias53 Syncope Mimics Syncope mimics are conditions that share features with syncope and must be considered when evaluating patients who have fainted8,11 (See Table 6) Foremost among the syncope mimics are seizures It is very common for a syncope patient to have an initial ED chief complaint of “seizure” because a witness saw the individual’s eyes rolling back and limbs jerking The transient cerebral hypoxia of syncope will cause many patients to have myoclonic jerking that resembles seizure activity However, this involuntary motor activity generally will be briefer and more irregular than the tonic-clonic activity of a grand mal convulsion Urinary and fecal incontinence can occur with both seizures and syncope, but is seen more commonly with an epileptic event Fecal incontinence with fainting is exceedingly rare Another key differentiating feature is the lack of prolonged postictal obtundation or agitation after a faint Syncope patients may feel dazed and unwell and appear confused after the event, but normal consciousness will return within several minutes Children may feel fatigued and drowsy for half an hour or more after fainting Tongue biting can occur with syncope, but is more likely to be at the tip of the tongue than on the lateral aspect of the tongue, as seen after seizures This is because of a sudden mouth closure if the patient faints and hits his or her chin, as opposed to tonic-clonic clenching of the jaw during a seizure Seizures Metabolic disturbances Intoxication Psychiatric pseudo-seizures Large anterior circulation cerebrovascular accident Subarachnoid hemorrhage Basilar transient ischemic attacks Subclavian steal syndrome Thoracic aortic dissection Cataplexy Carotid circulation TIAs and strokes do not cause bihemispheric perfusion deficits and, in theory, should not result in a true syncopal event But major cerebrovascular accidents (CVAs), such as a large vessel occlusion, an intraparenchymal bleed, or subarachnoid hemorrhage, often are heralded by a transient loss of consciousness Unlike patients with syncope, these patients will not return to baseline mental status but typically will have neurologic deficits, altered mental status, or severe headache Posterior circulation TIAs and strokes may cause a transient loss of consciousness via a circulatory insult to the brainstem reticular activating system23 Basilar vascular events typically are accompanied by neurologic signs and symptoms of varying severity, such as ataxia, diplopia, dysphagia, hemiparesis, paresthesias, vertigo, and headache However, basilar TIAs may result in syncope without lingering posterior fossa neurologic signs The subclavian steal syndrome can cause syncope This uncommon condition involves an occlusion of the subclavian artery proximal to the vertebral artery When the ipsilateral arm is exercised, retrograde flow down the vertebral artery supplies the excess demand and can result in brainstem ischemia and occasionally syncope It usually is asymptomatic but can cause symptoms, especially in people who work with their arms raised above their heads Episodes of vertigo occur in about half of these individuals as well Patients with subclavian steal will have a blood pressure differential from one arm to the other Another vascular disorder that can result in syncope is aortic dissection As the dissection wave proceeds between the wall layers, it can impinge upon the carotid and vertebral arteries, thus impairing cerebral or basilar circulation, respectively Patients generally have chest pain radiating into the back Metabolic and toxic events, such as hypoglycemia, hypoxia, carbon monoxide poisoning, sepsis, or respiratory alkalosis secondary to hyperventilation, along with various intoxications, can result in episodes of transient loss of consciousness The clinician usually will have ample clues to help differentiate these conditions from that of a classic syncopal episode, including laboratory and vital sign abnormalities, lingering mental status changes, or obtundation Some individuals experiencing hypoglycemia, especially diabetes patients being treated with insulin, will have fainting events followed by a return to near baseline mental status34 For this reason, it is reasonable to perform bedside glucose testing on patients with otherwise unexplained syncope, especially those patients with diabetes Cataplexy also may mimic a syncopal episode Rarely seen except in patients with narcolepsy, a cataplexy event usually is triggered by intense emotion, such as anger, fear, or laughter It involves a sudden transient loss of muscle tone that may be mild or severe enough to make the patient collapse The key feature distinguishing it from syncope is that patients experiencing a cataplexy episode will not lose consciousness34 As many as 70% of patients with narcolepsy can experience cataplexy spells Psychogenic pseudosyncope can mimic both cataplexy and syncope Its characteristics are described in the section on syncope in children In older literature, the term “drop attack” often is listed under the heading of syncope mimics A “drop attack” generally refers to a sudden fall without loss of consciousness Used to describe events caused by many conditions, including orthopedic, cardiac, and neurologic events, the term is ambiguous, and the clinician is better served by more specific descriptors of such episodes History A good history, obtained from the patient and any available witnesses, remains vital to the evaluation of syncope, and will suggest the most likely diagnosis in 50% or more of cases9 The first step involves confirming that the event really was syncope and was not a seizure The loss of consciousness of syncope usually is less than a minute and full consciousness is regained quickly Involuntary myoclonic motor activity is common with syncope but usually quite brief Urinary incontinence may occur with syncope, but occurs less often than during a seizure The next step is to gather as much information as possible about the setting, the presence of a prodrome, and other situational and historical data Was there a possible triggering event, such as standing for a long time in a warm environment or the sight of blood? Was the event postural in nature? Was the patient looking up or wearing a tight collar? Was there some reason the patient might have been poorly hydrated, such as working outside on a hot, humid day without much fluid replenishment? Was there a prodrome of nausea, diaphoresis, and lightheadedness, and how long did the prodrome last? Syncope without warning raises the red flag for a cardiac cause (See Table 5) Palpitations, chest pain, and the occurrence of fainting during exertion or while supine also suggest a cardiac cause, either ischemic, dysrhythmic, or structural Syncope with dyspnea raises concern for a pulmonary embolism, chest pain for MI or dissection, headache for subarachnoid hemorrhage, back pain for aortic dissection, abdominal pain for ruptured abdominal aortic aneurysm, and pelvic pain for a ruptured ectopic pregnancy If the patient was exercising an arm when the event occurred, consider subclavian steal syndrome Focus past history on the existence of previous similar events and the presence of underlying structural, valvular, or atherosclerotic cardiac disease and or any comorbidities such as congestive heart failure, diabetes, hypertension, thromboembolic disorder, or parkinsonism The patient’s medication list should be reviewed for drugs such as diuretics, beta-blockers, calcium channel blockers, and other arrythmogenic or vasoactive agents Has there been a recent change in medications? Had the patient been using alcohol or any illicit substances prior to the event? For family history, are there any instances of sudden death at a young age to suggest an occult congenital condition, such as the long QT syndrome or Brugada syndrome? Physical Exam Features Vital sign abnormalities may yield clues immediately to the nature of the syncopal episode, such as slow or rapid heart rates pointing toward an arrhythmic event, hypoxia and tachypnea suggesting a pulmonary embolism, or the presence of a fever Orthostatic blood pressure measurement is warranted in most syncope patients An altered sensorium raises concern for toxic or metabolic insults, cerebrovascular accidents, or postictal states and may be seen in aortic dissection as well Cardiovascular examination focuses on identifying cardiac murmurs, signs of congestive failure, or unequal extremity pulses A rigid, tender abdomen may herald a ruptured ectopic or abdominal aortic aneurysm Search for neurologic deficits, including posterior fossa signs such as vertigo, abnormal nystagmus, diplopia, and ataxia If anemia is suspected, a rectal exam to check for gastrointestinal bleeding may be warranted The physical exam also should evaluate for signs of trauma In elderly patients who have fallen, assume that syncope might have precipitated the fall, unless the history clearly indicates that the fall was mechanical in nature The same holds true for individuals involved in otherwise unexplained motor vehicle accidents If an individual receives injuries during a syncopal event that suggest they did nothing to try and protect themselves during a fall, it goes against the likelihood of the event being a psychogenic pseudoseizure Testing Strategies An ECG is the only test that should be performed on all syncope patients41 Although it usually will be normal, the ECG is a quick, inexpensive, and noninvasive risk-stratification tool Analyze the ECG for obvious rhythm disturbances (bradycardia, atrial fibrillation, ventricular fibrillation) and signs of ischemia or myocardial damage, along with conduction abnormalities including AV blocks Search for either short QT interval (QTc < 350 milliseconds [ms]) or long QT interval (QTc > 450 ms in males, > 470 ms in females) New or old left bundle branch block patterns and anterior or posterior fascicular block are associated with greater morbidity in the setting of syncope41 Also evaluate all ECGs for the right bundle branch block, ST elevation pattern of Brugada The need for laboratory testing or imaging is driven by the clinical situation26,41 All reproductive-capable females who experience syncope should have a pregnancy test Concern for anemia requires a complete blood count Patients with diabetes should have their glucose tested A chemistry panel is warranted if there is a possibility of electrolyte abnormality Chest pain or ECG changes suggest the need for troponins Patients at low probability for pulmonary embolism can be risk-stratified with a D-dimer assay Go straight to CT angiography for patients at moderate to high risk for pulmonary embolism or for patients in whom the diagnosis of thoracic aortic dissection is being considered Carotid or vertebral artery dissections are a rare cause of syncope, but in patients with syncope and neck pain or injury, CT angiography of the neck is indicated Cardiac echocardiogram is mandated at some point for patients whose syncope may have arisen from structural heart conditions, such as valvular disease, atrial myxoma, or hypertrophic cardiomyopathy Tilt table testing can elucidate the cause of recurrent neurally mediated or postural syncope, although this seldom if ever will be performed in the ED26 Evaluation for arrhythmogenic cardiac syncope warrants a period of cardiac monitoring If the patient meets high-risk criteria, as discussed below, this should be done in the inpatient setting Other things being equal, lower-risk patients sometimes may be discharged safely from the ED with portable short-term cardiac monitoring devices (Holter) and firm follow-up instructions For patients with recurrent unexplained syncope, implantable loop recorders have shown promise54,55 Carotid sinus massage, the technique that has been described previously, can be used to diagnose carotid sinus hypersensitivity, but is seldom used in the ED This has less to do with the rare but potentially catastrophic danger of causing a CVA, and relates more to the high rate of false positives41 Unless the history and examination suggest head trauma or a CVA, routine CTs of the head are not indicated in patients with no further symptoms after an isolated syncopal event41 To address the issue of ED over-admission of syncope patients who cannot be diagnosed with a benign cause for the event,41 several clinical decision-making rules have been developed over the past 15 years to risk stratify patients (See Table 7) One of the earliest and most extensively validated tools is the San Francisco Syncope Rule (SFSR), published in 200456 Against an outcome measure of serious events at seven days (including death, MI, PE, CVA, arrhythmias, subarachnoid hemorrhage, significant hemorrhage, and related return ED visits or readmission), the SFSR assessed the predictive value of the following variables in patients with syncope or presyncope: abnormal ECG, history of congestive heart failure and hematocrit < 30%, dyspnea, and systolic blood pressure < 90 mmHg A subsequent meta-analysis of studies using the SFSR suggested that in patients whose syncope remains undiagnosed after ED evaluation, the presence of one of these variables yields a sensitivity of 087 in predicting an adverse outcome57 The original SFSR investigators calculated that application of the rule could reduce admission rates safely by 10%9 Name Variables Results Sensitivity San Francisco Syncope Rule 56 Abnormal electrocardiogram Congestive heart failure history Hematocrit Dyspnea Systolic blood pressure < 90 mmHg Consider admission if one or more variables is present 87% (conflicting internal and external validations) Boston Syncope Criteria 15 Volume depletion Abnormal vital signs or patient is symptomatic or has an abnormal exam Acute coronary syndrome Conduction disease Worrisome cardiac history Family history of sudden death Central nervous system event Valve disease by history or on exam Consider admission if one or more variables is present 97% (small sample internal validation) Risk Stratification Of Syncope in the Emergency Department (ROSE) 60 Hemoglobin < 9 g Brady < 50 beats per minute B-type natriuretic peptide (BNP) > 300 ng/L Chest pain Q waves (except lead III) O2 sat < 94% Fecal occult blood (if gastrointestinal bleed is suspected) Consider admission if one or more variables is present 87% (small sample internal validation) The most recently published set of syncope guidelines is the Canadian Syncope Risk Score, which was published in 2016 and has not yet been fully validated58 In this prospective observational study of more than 4,000 patients — the largest study yet involving risk stratification in syncope — researchers assigned positive or negative values to various clinical features in a cohort of patients 16 years of age and older Positive predictors of adverse outcomes include: history of heart disease and any systolic pressure < 90 mmHg or > 180 mmHg and elevated troponin levels and abnormal QRS axis and QRS > 130 ms and QTc > 480 ms and and an ED diagnosis of cardiac syncope Negative values were assigned to two additional factors: a patient’s predisposition to vasovagal symptoms and an ED diagnosis of vasovagal syncope One of the interesting features of this study is that it incorporates clinical judgment into the scoring paradigm This integrates the findings from a meta-analysis of several syncope rules, which suggested that clinical judgment is as sensitive as any rules yet developed in predicting adverse outcomes in syncope59 The total points in the Canadian Syncope Risk Score stratify patients into categories ranging from very low risk to very high risk This is now in the process of being validated The evaluation of patients with syncope remains a frequent challenge facing emergency physicians Careful history taking, examination, and the judicious use of testing, if needed, will allow physicians to diagnose many patients with benign, neurally mediated, reflex syncope events But at least half the patients seen in the ED with syncope will receive no definite diagnosis41 A small percentage of them will have fainted because of immediate life-threatening conditions, such as acute coronary syndromes, malignant arrhythmias, pulmonary embolism, aortic dissection, subarachnoid hemorrhage, and other catastrophic conditions As long as physicians remain alert for the red flags of abnormal vital signs and associated symptoms, such as dyspnea, headache, and chest pain, these conditions are relatively easy to suspect But a certain percentage of patients will have cardiac syncope because of factors that will not be obvious during the ED evaluation, and these patients have the potential for adverse events if discharged with an incomplete evaluation The use of syncope risk stratification guidelines can help make rational admission decisions, although as of yet they do not replace the gestalt of experienced clinicians, who will be aware of the following high-risk features and incorporate them into their decision making: syncope without a prodrome and syncope accompanied by chest pain, shortness of breath, or palpitations and syncope during activity and syncope while supine and a history of CHF, coronary artery disease, or other cardiac conditions, including valvular disease and abnormal ECG findings, as discussed previously and the presence of anemia and family history of sudden death at a relatively young age and hypotension or hypertension and and age older than 60 years 1 De Lorenzo RA Chapter 15: Syncope In: Marx J, Hockberger R, Walls R Rosen’s Emergency Medicine – Concepts and Clinical Practice 8th ed Philadelphia: Elsevier and 2014 2 Bennett MT, Leader N, Krahn AD Recurrent syncope: Differential diagnosis and management Heart 2015 and 101:1591-1599 3 Angus S The cost-effective evaluation of syncope Med Clin North Am 2016 and 100:1019-1032 4 Osler W The Principles and Practice of Medicine, 8th Edition, New York and London: D Appleton and Company and 1918: 983 5 Sheldon RS, Morillo CA, Krahn AD, et al Standardized approaches to the investigation of syncope: Canadian Cardiovascular Society position paper Can J Cardiol 2011 and 27:246-253 6 Eskin B, Allegra JR Inpatient admission rates for syncope vary among and within countries: A meta-analysis Ann Emerg Med 2014 and 64:S74 7 Kidd SK, Doughty C, Goldhaber SZ Syncope (fainting) Circulation 2016 and 133:e600-e602 8 Brignole M, Moya A, de Lange FJ, et al 2018 European Society of Cardiology guidelines for the diagnosis and management of syncope Eur Heart J 2018 and 39:1883-1948 9 Runser LA, Gauer RL, Houser A Syncope: Evaluation and differential diagnosis Am Fam Physician 2017 and 95:303-312 10 Brignole M, Hamdan MH New concepts in the assessment of syncope J Am Coll Cardiol 2012 and 59:1583-1591 11 Weimer LH, Zadeh P Neurological aspects of syncope and orthostatic intolerance Med Clin North Am 2009 and 93:427-449 12 Benditt DG, Nguyen JT Syncope: Therapeutic approaches J Am Coll Cardiol 2009 and 53:1741-1751 13 Adkisson WO, Benditt DG Syncope due to autonomic dysfunction: Diagnosis and management Med Clin North Am 2015 and 99:691-710 14 MacNeill EC, Vashist S Approach to syncope and altered mental status Pediatr Clin North Am 2013 and 60:1083-1106 15 Grossman SA, Fischer C, Lipsitz LA, et al Predicting adverse outcomes in syncope J Emerg Med 2007 and 33:233-239 16 Quinn JV Syncope and presyncope: Same mechanism, causes, and concern Ann Emerg Med 2015 and 65:277-278 17 Thiruganasambandamoorthy V, Stiell IG, Wells GA, et al Outcomes in presyncope patients: A prospective cohort study Ann Emerg Med 2015 and 65:268-276 18 Grubb BP Clinical Practice Neuro-cardiogenic syncope N Engl J Med 2005 and 352 and 10:1004-1010 19 Adkisson WO, Benditt DG Patho-physiology of reflex syncope: A review J Cardiovasc Electrophysiol 2017 and 28:1088-1097 20 Tan MP, Parry SW Vasovagal syncope in the older patient J Am Coll Cardiol 2008 and 51:599-604 21 Cotton TF, Lewis T Observations upon fainting attacks due to inhibitory cardiac impulses Heart 1918 and 7:23-24 22 Lewis T Lecture on vasovagal syncope and the carotid sinus mechanism, with comments on Gowers’s and Nothnagel’s syndrome BMJ 1932 and 1:873-876 23 Franco Folino A Cerebral autoregulation and syncope Prog Cardiovasc Dis 2007 and 50:49-80 24 Alboni P The different clinical presentations of vasovagal syncope Heart 2015 and 101:674-678 25 Chen-Scarabelli C, Scarabelli TM Neurocardiogenic syncope BMJ 2004 and 329:336-341 26 Writing Committee Members, Shen WK, Sheldon RS, Benditt DG, et al 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines and the Heart Rhythm Society Heart Rhythm 2017 and 14:e155-e217 27 Varosy PD, Chen LY, Miller AL, et al Pacing as a treatment for reflex-mediated (vasovagal, situational, or carotid sinus hypersensitivity) syncope: A systematic review for the 2017 ACC/AHA/HRS guideline for the evaluation and management of patients with syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society Circulation 2017 and 136:e123-e135 28 Saqr L, Kumar MM Case report: Neurocardiogenic syncope in the obstetric patient Anaesthesia 2007 and 62:79-84 29 Wieling W, Krediet CT, Solari D, et al At the heart of the arterial baroreflex: A physiological basis for a new classification of carotid sinus hypersensitivity J Intern Med 2013 and 273:345-358 30 Krediet CT, Parry SW, Jardine DL, et al The history of diagnosing carotid sinus hypersensitivity: Why are the current criteria too sensitive? Europace 2011 and 13:14-22 31 Hu ZW, Wang ZG, Zhang Y, et al Gastroesophageal reflux in chronic cough and cough syncope and the effect of antireflux treatment: Case report and literature review Ann Otol Rhinol Laryngol 2014 and 123:719-725 32 Thiagarajah PH, Finkielstein D, Granato JE Sitcom syncope: A case series and literature review of gelastic (laughter-induced) syncope Postgrad Med 2010 and 122:137-144 33 Evans WN, Acherman R, Kip K, Restrepo H Hair-grooming syncope in children Clin Pediatr 2009 and 48:834–836 34 Freeman R Syncope In: Jameson JL, Fauci AS, Kasper DL, et al, eds Harrison’s Principles of Internal Medicine, 20e New York: McGraw-Hill and 2018 35 Wieling W, Thijs RD, van Dijk N, et al Symptoms and signs of syncope: A review of the link between physiology and clinical clues Brain 2009 and 132:2630-2642 36 Klein LJ, Saltzman HA, Heyman A, Sieker HO Syncope induced by the Valsalva maneuver A study of the effects of arterial blood gas tensions, glucose concentration and blood pressure Am J Med 1964 and 37:263-268 37 Stewart JM Postural tachycardia syndrome and reflex syncope: Similarities and differences J Pediatr 2009 and 154:481-485 38 Folino AF Cerebral autoregulation in neurally mediated syncope: Victim or executioner? Heart 2006 and 92:724-726 39 Jansen RW Postprandial hypotension: Simple treatment but difficulties with the diagnosis J Gerontol A Biol Sci Med Sci 2005 and 60:1268-1270 40 Pilcher TA, Saarel EV A teenage fainter (dizziness, syncope, postural orthostatic tachycardia syndrome) Pediatr Clin North Am 2014 and 61:29-43 41 Quinn J Syncope In: Tintinalli JE, Stapczynski J, Ma O, et al, eds Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e New York: McGraw-Hill and 2016 42 Soteriades ES, Evans JC, Larson MG, et al Incidence and prognosis of syncope N Engl J Med 2002 and 347:878-885 43 Nishijima DK, Lin AL, Weiss RE, et al ECG predictors of cardiac arrhythmias in older adults with syncope Ann Emerg Med 2018 and 71:452-461 44 Bjerregaard P Diagnosis and management of short QT syndrome Heart Rhythm 2018 and 15:1261-1267 45 Polovina MM, Vukicevic M, Banko B, et al Brugada syndrome: A general cardiologist’s perspective Euro J Int Med 2017 and 44:19-27 46 Maron BJ, Ommen SR, Semsarian C, et al Hypertrophic cardiomyopathy: Present and future, with translation into contemporary cardiovascular medicine J Am Coll Cardiol 2014 and 64:83-99 47 Guimaraes RB, Essebag V, Furianetto M, et al Structural heart disease as the cause of syncope Braz J Med Biol Res 2018 and 51:e6989 48 Ball CA, Hegerova LT, Nkomo VT 23-year-old woman with syncope Mayo Clin Proc 2014 and 89:e93-97 49 Prandoni P, Lensing AW, Prins MH, et al Prevalence of pulmonary embolism among patients hospitalized for syncope N Engl J Med 2016 and 375:1524-1531 50 Zhang Q, Du J, Wang C, et al The diagnostic protocol in children and adolescents with syncope: A multi-centre prospective study Acta Paediatr 2009 and 98:879-884 51 Goldman RD Breath-holding spells in infants Can Fam Physician 2015 and 61:149-150 52 Raj V, Rowe AA, Fleisch SB, et al Psychogenic pseudosyncope: Diagnosis and management Auton Neurosci 2014 and 184:66-72 53 Hastings JL, Levine BD Syncope in the athletic patient Prog Cardiovasc Dis 2012 and 54:438-444 54 Solbiati M, Casazza G, Dipaola F, et al Cochrane corner: Implantable loop recorder versus conventional workup for unexplained recurrent syncope Heart 2016 and 102:1852-1863 55 Ruwald MH, Zareba W ECG monitoring in syncope Prog Cardiovasc Dis 2013 and 56:203-210 56 Quinn JV, Stiell IG, McDermott DA, et al Derivation of the San Francisco Syncope Rule to predict patients with short-term serious outcomes Ann Emerg Med 2004 and 43:224-232 57 Saccilott RT, Nickel CH, Bucher HC, et al San Francisco Syncope Rule to predict short-term serious outcomes: A systematic review CMAJ 2011 and 183:E1116-E1126 58 Thiruganasambandamoorthy V, Kwong K, Wells GA, et al Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope CMAJ 2016 and 188:E289-E298 59 Costantino G, Casazza G, Reed M, et al Syncope risk stratification tools vs clinical judgment: An individual patient data meta-analysis Am J Med 2014 and 127:1126e13-25 60 Reed MJ, Newby DE, Coull AJ, et al The ROSE (risk stratification of syncope in the emergency department) study J Am Coll Cardiol 2010 and 55:713-721
Emergency Medicine Reports, ISSN 0746-2506, 10/2018, Volume 39, Issue 19
AUTHOR Frank J. Edwards, MD, FACEP, Program Director, Emergency Medicine Residency, Arnot Ogden Medical Center, Elmira, NY PEER REVIEWER Steven M. Winograd,... 
Heart | Cardiac arrhythmia | Consciousness | Physicians | Systematic review | Emergency medical care | Patients | Posture | Hospitals | Etiology | Medical prognosis | Electrocardiography | Blood pressure
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