The older adult patient with syncope is one of the most challenging evaluations for the emergency physician. It requires clinical skill, patience, and knowledge of specific older adult issues. It demands care in the identification of necessary resources, such as medication review, and potential linkage with several multidisciplinary follow-up services. Excellent syncope care likely requires reaching out to ensure institutional resources are aligned with emergency department patient needs, thus asking emergency physicians to stretch their administrative talents. This is likely best done as preset protocols prior to individual patient encounters. Emergency physicians evaluate elders with syncope every day and should rise to the challenge to do it well.
Key points
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Mixed cause syncope occurs frequently in older adults, so the emergency physician should continue the evaluation to uncover multiple contributing causes and ensure complete care.
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Medications commonly contribute to syncope. The emergency physician should routinely review prescription medications especially if no cause of syncope is clear from emergency department (ED) evaluation.
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All forms of syncope can have recurrence in elder patients. Even “benign” neurally mediated syncope/vasovagal syncope recur, and this is associated with injury and functional decline. The emergency physician should initiate standardized patient education from the ED in all discharged elder syncope patients, to help prevent recurrence.
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Structural heart disease and congestive heart failure are strongly associated with cardiac syncope. Patients with this history are at high risk.
Introduction
Syncope is a sudden transient loss of consciousness (TLOC) and postural tone from rapid global cerebral hypoperfusion (RGCH) followed by full recovery to baseline function. Basing the definition of syncope on RGCH enables differentiation of syncope from other forms of TLOC, such as hypoxemia, hypoglycemia, seizure, vertebrobasilar ischemia, and psychogenic attacks. However, even elite medical publications apply variable definitions and inconsistent terminology for syncope, chiefly differing in the presence or absence of RGCH. Using this confusing definition in clinical practice causes a huge variability in evaluation, diagnosis, treatment, and disposition. For example, without RGCH, syncope can be confused with seizure, hypoxia, or hypoglycemia. If the definition does not require full recovery, then it can overlap with cerebral vascular accidents. The above confusion begins by using the term syncope as a diagnosis. However, syncope is not a diagnosis; it refers to the most dramatic presenting symptom of a variety of disease processes.
Emergency physicians evaluate the symptom of syncope in older adults on a daily basis. As with most emergent evaluations, the key tasks are to identify, stabilize, and admit life-threatening diagnosis, differentiate serious from benign causes in an efficient manner, risk stratify those who have an uncertain cause, and disposition patients to the appropriate subsequent level of care. This list of tasks is a tall order for the emergency provider because approximately 33% to 56% of syncope patients are discharged after a full hospital evaluation without definitive diagnosis. Therefore, emergency physicians must become skilled in the detection of causes, prognostication of risk, and ensuring appropriate disposition of this varied population of syncope patients.
Introduction
Syncope is a sudden transient loss of consciousness (TLOC) and postural tone from rapid global cerebral hypoperfusion (RGCH) followed by full recovery to baseline function. Basing the definition of syncope on RGCH enables differentiation of syncope from other forms of TLOC, such as hypoxemia, hypoglycemia, seizure, vertebrobasilar ischemia, and psychogenic attacks. However, even elite medical publications apply variable definitions and inconsistent terminology for syncope, chiefly differing in the presence or absence of RGCH. Using this confusing definition in clinical practice causes a huge variability in evaluation, diagnosis, treatment, and disposition. For example, without RGCH, syncope can be confused with seizure, hypoxia, or hypoglycemia. If the definition does not require full recovery, then it can overlap with cerebral vascular accidents. The above confusion begins by using the term syncope as a diagnosis. However, syncope is not a diagnosis; it refers to the most dramatic presenting symptom of a variety of disease processes.
Emergency physicians evaluate the symptom of syncope in older adults on a daily basis. As with most emergent evaluations, the key tasks are to identify, stabilize, and admit life-threatening diagnosis, differentiate serious from benign causes in an efficient manner, risk stratify those who have an uncertain cause, and disposition patients to the appropriate subsequent level of care. This list of tasks is a tall order for the emergency provider because approximately 33% to 56% of syncope patients are discharged after a full hospital evaluation without definitive diagnosis. Therefore, emergency physicians must become skilled in the detection of causes, prognostication of risk, and ensuring appropriate disposition of this varied population of syncope patients.
Epidemiology
The true incidence of syncope is difficult to estimate because of the noted variation in its definition as well as differences in prevalence, and underreporting in the general population. In the Framingham study, the age-adjusted incidence of syncope is 7.2 per 1000 person-years among both men and women. The lifetime cumulative incidence of syncope in women is almost twice that of men. The median peak of first syncope occurs around 15 years. The incidence rates increase with age, with a sharp increase at 70 years. The increased risk of syncope in elder patients appears to be due to age and disease-related abnormalities that impair the normal response to certain physiologic stresses. The age-adjusted incidence in patients with cardiovascular disease is nearly twice that of patients without cardiovascular disease. In the Framingham study, cardiac syncope increased the risk of nonfatal and fatal cardiovascular events and doubled the risk of death from any cause as compared with those without syncope. However, syncope itself does not increase risk of overall cardiac events or death except in the presence of heart disease, especially congestive heart failure (CHF). Patients with cardiac comorbidities are at increased risk of death after a syncopal event.
In the emergency department (ED), syncope is responsible for 1% to 3% of all patient visits and 6% of total hospital admissions. The elder population experiences disproportionately high hospitalization rates that increase by decade of life, with 58% of those over the age of 80 years admitted to the hospital when they present with the chief complaint of syncope. The distributions of syncope causes in elder patients are divided as shown in Fig. 1 .
The epidemiology of syncope varies significantly with age. The primary causes of syncope in older adults are neurally mediated syncope (NMS) (which in the Fig. 1 includes orthostatic hypotension [OH]), carotid sinus hypersensitivity (CSH), and dysrhythmias. OH can be classed as a subtype of NMS or stand alone. In all of these classifications, syncope results from the lowering of peripheral resistance and/or cardiac output (CO). NMS, inclusive of vagal, carotid, and situational events remains the most common cause of syncope even in the elder population. OH causes syncope in 20% to 30% of older adults. Cardiac dysrhythmia incidence dramatically increases with age. Prevalence in patients over the age of 80 years is nearly 9% for atrial fibrillation/flutter alone. Anyone with a history of rheumatic fever, CHF, or hypertension is at greater risk for a cardiac dysrhythmia as cause of syncope.
Syncope can be remarkably debilitating and is associated with more than $2 billion in annual health care costs, and a mean cost of $5,400 per hospitalization. Despite this high cost and resource utilization, the morbidity and mortality of syncope, including those of cardiac cause, is minimally impacted by health care interventions. Up to 60% of admitted syncope patients are discharged without receiving any therapeutic intervention for syncope.
Pathophysiology
Once again, it can be seen why an important part of the syncope definition is that it results from RGCH. An approximate 20% drop in cerebral oxygen delivery is sufficient to cause loss of consciousness (LOC). Cerebral perfusion pressure is dependent on mean arterial pressure, which is in turn dependent on CO and peripheral vascular resistance (PVR). The pathophysiology is not yet entirely known, and a topic of continued research, but it appears that alterations in CO and PVR contribute to most cases of syncope.
NMS is due to abnormal autonomic regulation, resulting in hypotension, bradycardia, and ultimately, LOC. Humans have the exceptional ability to maintain stable blood pressures during physiologic stress and shifting fluid volumes through changes in vascular tone and CO. Decreased output sensed by arterial baroreceptors in the carotid sinus and aortic arch increase sympathetic output, resulting in increased heart rate and ventricular contractility. In addition, the vascular system responds by limiting blood flow to nonessential organs, thereby increasing PVR and causing a gradual increase in diastolic pressure. In NMS, an abnormal autonomic nervous system overresponds to different stimuli, most commonly prolonged standing, heat, emotional stress, or carotid sinus stimulation. These stimuli increase heart rate and ventricular contraction. However, by unclear mechanism, neural signals reach the brainstem and result in a combination of sympathetic withdrawal and increased parasympathetic output, instead leading to bradycardia, hypotension, and syncope. Decreased venous filling due to hypovolemia from volume loss, inadequate intake, or medication effects causes OH. It can also be due to autonomic dysfunction. Cardiogenic syncope is due to structural heart diseases or dysrhythmias. Both impair CO and thus cerebral perfusion.
Aging patients are more prone to syncope because of the following:
- 1.
Reductions in cerebral blood flow, CO, and thirst
- 2.
Altered homeostasis of water and salt in the renal system
- 3.
Altered baroreceptor function, diminished heart rate, and vasoconstriction response
- 4.
Structural heart disease
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The impaired diastolic filling and stroke volume with normal aging
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Autonomic dysfunction
- 6.
Polypharmacy
Cause and classification of syncope
Main Causes of Syncope
Three main categories encompass most syncope causes: they are most commonly NMS, followed by OH, then cardiac cause. Mixed cause syncope is common in the older adult, but its exact incidence is not clear. It is therefore important to note that older patients may often have multifactorial causes of syncope. Emergency physicians, however, often stop once a single attributable cause has been identified; this fails to identify mixed cause syncope. Physicians should consider multiple causes in all patients with syncope. The most high-yield secondary causes are medication effect and comorbidities. Always consider these as causes of multifactorial syncope.
- 1.
NMS includes functional disruption of CO by bradycardia or vasodilation; this is also termed reflex syncope. The mechanisms involved are divided into vasovagal syncope (VVS), situational, or carotid sinus sensitivity.
- a.
VVS is the single largest cause of syncope. In this situation, syncope is triggered by an event such as pain, emotional upset, fear, or prolonged standing. Onset is associated with typical prodromal symptoms of diaphoresis, nausea, tunnel vision, and then LOC. VVS requires an intact autonomic nervous system, and therefore, should never be diagnosed in patients with autonomic dysfunction.
- b.
Situational syncope follows specific events of micturition, defecation, coughing, laughing, or swallowing. However, lack of cerebral perfusion may wipe the memory of this precipitating event away and confound the history.
- c.
CSH is an exaggerated response from stimulation of the carotid sinus causing asystole. It can be isolated or exist as part of a generalized autonomic disorder. It is most common in men and is often associated with falls, placing patients at higher risk for injury and fractures.
- a.
- 2.
OH can be included under the category of NMS syncope. It can also be classed alone when it occurs from simple volume depletion such as poor intake, gastrointestinal (GI) loss, or hemorrhage. Drugs from several classes may also cause OH by lowering PVR. Finally, OH occurs when the normal autoregulatory processes of vasoconstriction and reflex heart rate increase fail to occur. OH can be a result of primary autonomic failure from neurodegenerative disease or secondary autonomic failure from other systemic diseases like diabetes, hepatic or renal failure, and chronic alcohol abuse. OH is an example of a geriatric syndrome and may be seen as part of the systemic dysregulation that occurs in frailty. The clinical symptoms and signs of OH depend on its cause and severity. OH as a geriatric syndrome is a predictor of poor prognosis.
- 3.
Cardiac causes of syncope occur as decreased CO causes hypoperfusion. Events are either electrophysiological as in dysrhythmia, structural, or related to cerebrovascular steal syndromes.
- a.
Dysrhythmias include atrial fibrillation and flutter, high-grade atrioventricular (AV) block, ventricular tachycardia, sinus node dysfunction, sick sinus syndrome, and pacemaker dysfunction. The causes of the rhythm disturbance itself are most commonly ischemic, followed by hypertensive disease.
- b.
Structural heart disease, such as valvular stenosis, cardiomyopathies, cardiac masses, and pericardial effusions or other outflow obstructions.
- c.
Cerebrovascular steal syndromes occur when distal obstruction of an artery prevents normal forward flow, leading to retrograde flow, resulting in ischemia distal to the involved artery. These very rarely occur without associated focal neurologic deficits or seizurelike activity.
- a.
- 4.
Multifactorial syncope is common in older adults and is an independent risk for adverse outcomes. When several causes may be in play simultaneously, consider this a high-risk patient and investigate multiple causes even when the first most likely cause has already been found.
Unlikely Causes of Syncope
Transient ischemic attacks
Transient ischemic attacks (TIAs) do not cause true LOC. The only possible exception is a TIA affecting the vertebrobasilar circulation. In this situation, other signs such as paralysis, eye movement disorders, and vertigo, should be noted by history or physical examination. Any syncopal events without these associated symptoms are not due to cerebrovascular ischemia, and typical syncope patients do not warrant a TIA evaluation.
Psychogenic syncope
These episodes do not fit the full definition of syncope because LOC here is not caused by RGCH. However, up to 20% to 35% of more loosely defined syncope patients may have psychogenic syncope and require psychiatric evaluation to determine this cause. Emergency physicians should consider a psychiatric cause of these TLOC events that look like syncope. Understanding this distinction may result in better diagnosis and treatment.
Diagnostic evaluation
History
The main goal in syncope evaluation is differentiating benign versus life-threatening causes. The single most important tool in the syncope evaluation is a good history. A complete syncope history can reduce the need for additional testing, decrease costs, shorten ED stays, and improve patient satisfaction. A detailed syncope history may be the key to distinguishing benign from more concerning causes.
Step 1 is to establish syncope as a TLOC of rapid onset and short duration, with a complete and spontaneous recovery to presyncope level of function. Beginning with an inconsistent definition leads to inappropriate diagnostic testing and inconsistent treatment. The American College of Cardiology and the American Heart Association use the broader classification of syncope, whereas the European Society of Cardiology (ESC) definition is narrower. Specific features may be difficult to establish by history, because cerebral hypoperfusion may cause amnesia of the event. In fact, 40% of elder patients have complete amnesia of a syncopal event. Further complicating the history, witnesses to the event may not be present or may report inconsistent accounts. Moreover, syncope is often difficult to differentiate from seizure because of the convulsive activity seen in 4% to 40% of syncopal events. LOC in syncope is due to RGCH, whereas in seizure, it is due to abnormal electrical activity. To facilitate this often difficult distinction, Sheldon created a history-based scoring system that can differentiate between the 2 with a sensitivity and specificity for seizures of 94%. A history of tongue biting and confusion following the episode is more indicative of seizure, whereas light-headedness, sweating, and prolonged standing are more predictive of syncope ( Table 1 ).
| Question | Points |
|---|---|
| Any tongue biting? | 2 |
| Any sense of déjà vu before the episode? | 1 |
| Association with emotional stress? | 1 |
| Anyone notice head turning during event? | 1 |
| Any unusual posturing, jerking limbs, or lack of memory afterwards? | 1 |
| Any confusion afterwards? | 1 |
| History of lightheaded episodes? | −2 |
| Sweating before episodes? | −2 |
| Any prolonged standing or sitting? | −2 |
History of present illness
Classically, VVS features a prodrome of warmth, nausea, sweating, and light-headedness. Syncope without prodrome, or when associated with palpitations, supine position, or exercise, is concerning for cardiac cause. It is also important to investigate for concurrent infection or illness, especially symptoms consistent with hypovolemia, such as vomiting, diarrhea, bleeding, and decreased appetite that may point to OH. The clinician should elicit any associated straining or coughing that could point to a situational cause and obtain any history of prior episodes. Evaluate medications for agents such as diuretics, antihypertensives, and others that may affect volume status, autonomic stability, or cardiac function. Inquire regarding any medication dose changes, new medications, and recent alcohol or drug use. Recent bed rest and deconditioning can also cause OH.
Past medical history
After discussing the current episode, it is important to further risk stratify using the patient’s past medical history. Obtain any history of heart failure, myocardial infarction, structural heart disease, and family history of heart disease or sudden death. Some common features that are predictive of low mortality following syncope are history not consistent with cardiac, abdominal, or focal neurologic symptoms; a normal physical examination; no evidence of CHF; no new neurologic deficits; normal glucose; and benign EKG. In this study, there were no deaths or adverse outcomes in patients discharged from the ED who met these criteria.
Heart disease is an independent predictor of cardiac syncope (odds ratio 16, P = .00001), with a sensitivity of 95% and a specificity of 45%. In contrast, the absence of heart disease excludes a cardiac cause of syncope in 97% of the patients. Also, solicit illnesses with dysautonomia such as Parkinson disease, multiple sclerosis, alcohol abuse, and diabetes.
Medications
Medications are a major issue in the evaluation of syncope. OH alone may be caused by a long list of medications including diuretics causing volume depletion, α-blockers for benign prostatic hypertrophy (BPH), sympatholytics and vasodilators impairing autonomic response, anti-Parkinson medications, tricyclics, atypical antipsychotics, and monoamine oxidase inhibitors. A careful review of medications is needed, and if suspected as a cause of syncope, consultation with a pharmacologist may be helpful.
Structured syncope history
- 1.
Define history of true syncope with global cerebral hypoperfusion
- 2.
Distinguish from other transient LOC events (ie, seizure)
- 3.
Treat near syncope the same as full syncope
- 4.
Define precise details of the event/chief complaint
- a.
Ask what the patient was doing at the time
- b.
Ask about provocative triggers
- c.
Ask if any prodromal symptoms occurred
- d.
Establish series of events
- e.
Determine duration of LOC
- f.
Ask if associated symptoms occurred
- g.
Ask if there is a current contributory illness/event (flu, fever, bleeding)
- h.
Ask if there are symptoms of OH or autonomic dysfunction
- a.
- 5.
Are there active traumatic complaints or risk of trauma
- 6.
Specifically question any fall and falls in the prior year
- 7.
Obtain a focused past medical history
- a.
Prior syncope and its diagnosis
- b.
Cardiovascular disease
- c.
GI losses especially hemorrhage
- d.
Diseases with autonomic failure
- a.
- 8.
Medications: specifically review for drug effect syncope; class IA and IC antiarrhythmics are common causes of syncope; anticoagulants are critical if concurrent trauma exists
Physical Examination
After a careful history, conduct a thorough physical examination. First, examine the vital signs, including orthostatic vital signs. Abnormal vital signs need to be addressed and warrant explanation. Those with persistent (>15 minutes) abnormal vitals are at higher risk for adverse outcome. Furthermore, a careful cardiopulmonary examination should be done to evaluate for signs of heart failure or structural heart disease. Take note of any pericardial rubs, murmurs, extremity edema, jugular venous distension, or rales. Neurologic examination should evaluate for focal deficit or altered mentation. Focal neurologic examination may suggest an alternate diagnosis and should be further evaluated. Because tongue biting is very specific (96%) for seizure, it is useful to examine the tongue. A rectal examination for fecal occult blood should be performed if GI bleeding is a concern. It is also important to evaluate for signs of trauma, which accompany 39% of syncopal episodes in the older patient.
Testing
Initial testing will depend largely on information gathered on history and physical examination, with few exceptions. One exception is that all patients with syncope should have a 12-lead electrocardiogram (EKG) performed in the initial evaluation.
Electrocardiogram
The EKG is fast, inexpensive, and safe. With an EKG, the clinician can assess for signs of structural heart disease and arrhythmia. The Ottawa EKG Criteria identify patients at risk for 30-day serious cardiac outcome. Positive findings are second-degree Mobitz type 2 or third-degree AV block, bundle branch block with first-degree AV block, right bundle branch with left anterior or posterior fascicular block, new ischemic changes, non-sinus rhythm, left-axis deviation, or ED cardiac monitor abnormalities. The sensitivity and specificity of the Ottawa EKG Criteria were 96% and 76%, respectively.
In addition, those with EKG showing any arrhythmia, premature atrial contraction, premature ventricular contraction, pacing, second- and third-degree AV blocks, and left bundle branch block may benefit from echocardiography. It is otherwise not useful in those with normal EKGs, who are unlikely to have structural heart disease. Another important EKG diagnosis is Brugada syndrome (BS) ( Fig. 2 ). BS is a channelopathy, caused by mutation in the cardiac sodium channel that can lead to tachyarrhythmia and sudden death in structurally normal hearts. It is characterized by signature ST elevation in the precordial leads. A coved-type ST-segment elevation (type I) in one of the right precordial leads (V1–2) is the basis for diagnosis. The saddleback type 2 and 3 Brugada patterns are suggestive, but not sufficient for diagnosis. The Brugada pattern type I occurs in between 0% and 0.3% of the population and is more common in Asians and in men.
Orthostatic vital sign evaluation
A simple addition to the syncope workup is orthostatic vital sign measurement in the well-appearing patient. OH is common in elders with a prevalence of 16.4% in community-dwelling patients and increasing to 50% in institutionalized patients. It is critical to find OH because it is an independent predictor of mortality and falls. OH is often overlooked, leading to falls, injury, recurrent syncope, loss of function, and even death. OH is the physical finding of a greater than 20-mm Hg decrease in systolic or greater than 10 mm Hg decrease in diastolic blood pressure within 3 minutes of standing. Standing causes decreased venous blood return because 25% to 30% of the systemic circulation begins pooling in the lower extremities. Subjective light-headedness within 2 minutes of standing is also considered OH. There can be wide variation in orthostatic vital sign changes for healthy and ill individuals alike, and there may be poor correlation of vital signs with level of dehydration. Nevertheless, positive orthostatic vital signs or those that reproduce symptoms can reinforce concerns about volume status or autonomic instability. OH is a common finding in elder patients. Older adults can have impaired ability to maintain blood pressure due to autonomic dysfunction, altered baroreceptor function, decreased cardiac contractility, and medication effects in addition to peripheral vascular disease. OH is present in up to 20% of patients older than 65 years, although as few as 2% of these patients were symptomatic, making it important to assess this finding when it is suspected.
Laboratory evaluation
Initial laboratory work should be catered to the individual patient. Routine blood work is low yield in the general evaluation of syncope. However, it is reasonable for all syncope patients to have a point-of-care glucose. This cheap, easy test can exclude an easily reversible cause of syncope. Patients with clinical evaluations or histories concerning for bleeding, acute coronary syndrome, or metabolic disturbance should be evaluated for such diagnoses. However, in elder patients, the history can be unrevealing or unobtainable, and the physical examination is often nonspecific. Therefore, clinicians should maintain high suspicion and order blood work on an individual basis. One test with high significance is the brain natriuretic peptide (BNP). Notably, elevation of the BNP has been associated with a significant increase in mortality.
Imaging
No imaging is routinely needed, again unless prompted by history or physical examination. Routine computed tomographic (CT) scans, echocardiography, carotid ultrasound, and electroencephalography all together affected diagnosis or management in less than 5% of cases and helped determine the cause of syncope less than 2% of the time. The American College of Emergency Physicians (ACEP) does not recommend routine CT head scan in asymptomatic adult patients with syncope, insignificant trauma, and a normal neurologic examination. Nonetheless, 39% of elder patients will present with trauma, which may necessitate individualized imaging.
Non-emergency department testing
Arrhythmia may be suspected in those syncopal patients with no prodrome, with palpitations or arrhythmia on EKG, specifically those included in the Ottawa EKG criteria. Patients with features concerning for arrhythmia should have telemetry monitoring. Following an ED telemetry observation period, some have proposed outpatient Holter monitoring as a safe, effective means to diagnose arrhythmogenic syncope. These devices are worn for 24 to 36 hours and should be considered in a carefully selected group of patients who otherwise do not appear to have a life-threatening condition and have frequent enough episodes that an event is likely to be detected during the Holter evaluation timeframe. External or implantable loop recorders are potentially more useful devices in the detection of symptomatic arrhythmia during longer timeframes. Those at higher risk according to physician judgment or decision rules should be admitted for telemetry monitoring.
A study by Kapoor and colleagues found that prolonged monitoring could identify various dysrhythmias, such as sinus bradycardia, supraventricular tachycardia, atrial fibrillation, ventricular tachycardia, or short sinus pauses. However, even in these patients with dysrhythmia, a definite cause of syncope was found in only 15% of subjects. Moreover, 1% to 4% of the normal populations exhibited asymptomatic periods of sinus pause, and up to 2% had short episodes of ventricular tachycardia. Given this, one must be mindful that some arrhythmia findings during monitoring may be incidental and not the cause of syncope.
Outpatient testing
Those discharged from the ED or from the hospital may require additional follow-up testing to clearly identify the cause of their syncope. Electrophysiology studies assess the integrity of the His Purkinje system. This study is rarely indicated for syncope, especially in those with a normal EKG and no structural heart disease. It is also not recommended for those with severe structural heart disease in which ICD instead is indicated. However, it may be reasonable in syncope patients with bifascicular block, when noninvasive tests fail to make the diagnosis.
Tilt-table testing is a common outpatient procedure in the syncope workup. Many protocols exist, but it generally consists of passive head-upright tilt for 20 to 60 minutes, which can produce hypotension, bradycardia, presyncope, or syncope. Sometimes patients are also given isoproterenol, sublingual nitrates, or clomipramine to further provoke symptoms. Tilt testing has been and remains a valuable tool for making correct and precise diagnoses of syncope and related conditions. It can be particularly helpful in distinguishing seizures versus syncope and diagnosing VVS, OH, postural orthostatic tachycardia syndrome, and psychogenic pseudosyncope.
Treatment
Although the emergency physician’s primary role in syncope is diagnosis, risk stratification, and determining safe disposition, it is important to be aware of some of the potential treatment modalities for syncope. Of course, specific interventions will be directed to the presumed or confirmed cause.
Neurally mediated syncope
The emergency physician’s most important role in the management of these patients is to diagnose the condition and educate the patient recognizing that patient misunderstanding and fear can severely impair quality of life and functioning. Education should include increased oral hydration and salt intake. This advice should be given with need to observe blood pressure elevation over time. Salt should be increased to 6 to 10 g of sodium chloride daily with 1.5 to 2 L of water. Physiologic counterpressure techniques, such as leg crossing and tensing calf muscles, are effective and can be done in any situation. The avoidance of trigger situations where identified should be advised. Finally, patients should be directed to lie flat at the onset of symptoms. Use of support stockings can alleviate symptoms and should be thigh or waist high to produce at least 15- to 20-mm Hg pressure.
It is critical to discontinue potentially offending medications; this may require pharmacology consultation, discussion with prescribing physicians, and ongoing patient evaluation. The emergency physician must take the time to ensure review of medications in every syncope patient. If the patient is to be discharged from the ED, it is critical for the emergency physician to ensure timely outpatient follow-up for ongoing evaluation and treatment. The primary goal is to reduce the incidence of recurrent syncope. In a structured follow-up setting, β-blockers, selective serotonin reuptake inhibitors, and midodrine have shown some potential benefit, especially in older patients with NMS. However, these medications are of questionable benefit and should not be initiated from the ED. Patients may also be referred for tilt-table testing, and consideration of pacemaker insertion if sinus arrest (carotid sinus syndrome) is the cause of NMS. It is important to note that pacemaker insertion has shown proven benefit for NMS. In addition, there is consensus regarding benefit of pacer insertion for patients in whom carotid sinus massage triggers symptoms. Table 2 demonstsrates vasovagal education.
