Download Syncope: Diagnosis and Evidence

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Coronary artery disease wikipedia , lookup

Electrocardiography wikipedia , lookup

Cardiac contractility modulation wikipedia , lookup

Myocardial infarction wikipedia , lookup

Management of acute coronary syndrome wikipedia , lookup

Arrhythmogenic right ventricular dysplasia wikipedia , lookup

Quantium Medical Cardiac Output wikipedia , lookup

Transcript
CASE-BASED REVIEW
Syncope: Diagnosis and Evidence-Based
Management
Case Study and Commentary, Shamai A. Grossman, MD, MS, and Rochelle Kohen, BS
Abstract
INSTRUCTIONS
Syncope accounts for nearly 3% of all emergency
department visits and 1% to 6% of all hospital admissions. Cardiac syncope patients have a mortality of 18%
to 33%; mortality for those with noncardiac or unexplained syncope is 3% to 4%. In addition, cardiac syncope is an independent predictor of mortality when
baseline cardiac conditions such as past congestive
heart failure or myocardial infarction are taken into
account. Determining the etiology of a syncopal event
is frequently difficult. It has been estimated that 30% to
50% of all cases of syncope cannot be given a definable
etiology even with extensive medical evaluation. Despite
increasing emphasis on evidence-based medicine,
efforts to reduce unnecessary and expensive medical
testing, and concerns over the rapidly rising costs of
medical care, syncope remains a frequent cause for
medical admission and costly clinical workup, and more
often than not a definitive diagnosis is not made. This
article reviews the approach to diagnostic testing and
management in the syncope patient.
The following article, “Syncope: Diagnosis
and Evidence-Based Management,” is a
continuing medical education (CME) article. To
earn credit, read the article and complete the
CME evaluation form on page 46.
S
yncope is common and often debilitating in patients of
all ages. It accounts for nearly 3% of all emergency department (ED) visits and 1% to 6% of all hospital admissions nationwide [1]. Syncope results from a brief loss in generalized cerebral blood flow [2]. It is defined as a transient loss
of consciousness producing a brief period of unresponsiveness and a loss of postural tone, ultimately resulting in spontaneous recovery requiring no resuscitation measures.
The causes of syncope range from the benign to the lifeendangering. Thus, it is critical for clinicians to appropriately evaluate and diagnose patients who present with this
symptom. Determining the etiology of a syncopal event,
however, is frequently difficult. Often the initiating event is
unwitnessed and not remembered by the patient, making it
difficult to uncover the specific circumstances leading up to
and occurring during the syncopal episode [3]. Syncopal
events are often transient and may resolve independently,
www.turner-white.com
OBJECTIVES
After participating in the continuing
education activity, primary care physicians
should be able to:
1. Be familiar with the clinical presentation of
syncope
2. Know the important elements in the history,
physical examination, and workup of syncope
patients
3. Identify common causes of syncope
4. Know the indications for hospital admission
following a syncopal event
without recurrence. It has been estimated that in 30% to 50%
of cases, the cause of syncope remains unexplained despite
extensive medical evaluation [4].
CASE STUDY
Initial Presentation
A 28-year-old woman who was found unconscious
at the bottom of an isolated stairwell in a local shopping mall is brought to the ED by emergency medical services (EMS). The patient, awake on EMS arrival, does not
recall the duration of her loss of consciousness nor the occurrences preceding the event. EMS reports no signs of confusion or lethargy.
From the Department of Emergency Medicine, Beth Israel Deaconess Medical
Center, Boston, MA.
Vol. 10, No. 1 January 2003 JCOM 39
SYNCOPE
Table 1. Diagnoses That Mimic Syncope
Seizure
Stroke
Coma
Subarachnoid hemorrhage
Physical Examination
Upon initial examination, the physician notes a blood pressure of 90/68 mm Hg, heart rate of 60 bpm, respiratory rate
of 18 breaths/minute, temperature of 96°F, and the presence
of anterior and lateral tongue lacerations. With the exception
of the lacerations and borderline low blood pressure, the patient has no other signs of trauma. The ED physician notes
no gross neurologic deficits.
• What are initial considerations in the patient with possible syncope?
• What factors support a diagnosis of syncope in this
patient?
The initial task is to obtain vital signs and determine the
need for immediate stabilization. The utility of orthostatic
vital signs is controversial, but they are probably helpful in
the elderly [5]. Measurement of blood pressure in both arms
may be useful to help evaluate for aortic dissection. Most
syncope patients are asymptomatic and have normal or
near normal vital signs. These patients do not need to be stabilized but require a thorough history and physical examination.
Other diagnoses can mimic syncope (Table 1), and in
approaching the syncope patient, one must first determine if
the event falls within the definition of syncope. Seizures and
stroke can cause loss of consciousness, but both can be distinguished from other etiologies of syncope by history and physical examination. Patients who have had a seizure often suffer
from metabolic acidosis [6]. Seizures classically present with
prodromal aura or “warning” symptoms and are typically followed by a postictal period in which the patient is often lethargic, agitated, and/or confused, with the patient slowly returning to full consciousness [7]. A loss of consciousness of greater
than 5 minutes’ duration and rhythmic movements can be
seen in both seizures and syncope but are far more common
in patients who have had a seizure [7]. Stroke, if associated
with loss of consciousness, will generally not be a self-limited
event but would tend to be of extended duration with focal
findings on neurologic examination [8].
Critical questions include the precipitating factor, such as
pain or anxiety, postural or exertional symptoms, the situa40 JCOM January 2003 Vol. 10, No. 1
tions in which episodesoccur (eg, after urination), associated
neurologic symptoms, history of cardiac disease, history of
psychiatric illness, medications being used, and a family history of sudden death [9].
Physical examination should include meticulous auscultation of the carotid arteries, heart, and lungs as well as careful palpation of the peripheral arteries. Evidence of trauma,
such as lacerations from tongue biting or contusions and
fractures, should be painstakingly noted.
In this patient, while the lateral tongue lacerations tend to
support the existence of tonic-clonic seizures, anterior lacerations are generally the result of a fall from syncope [10]. The
patient did not experience a prodrome nor were there focal
findings on neurologic exam. In addition, the event was selflimiting and without postictal confusion or agitation. These
aspects support a true syncopal episode.
Further History and Examination
The patient is otherwise healthy and not taking any
regular medications. She is a long-distance runner
but has been more easily tired of late and is no longer competing in races. She notes her last menstrual period was
approximately 8 weeks prior, but she has a lengthy history
of irregular menses. The patient denies intermittent vaginal
bleeding, spotting, lower abdominal pain, and cramping.
There was no clear precipitate or prodrome prior to the episode. There is no family history of sudden death or cardiac
disease. The patient was told previously that her blood pressure is low. On further examination, the physician notes a
systolic ejection murmur at the cardiac apex radiating to the
carotid artery.
Electrocardiogram (ECG) demonstrates normal sinus
rhythm with normal conduction intervals. A stool specimen
is examined for the presence of blood and is negative. A fingerstick test for glucose is negative for hypoglycemia and the
patient’s serum bicarbonate levels are normal. The results of
a urine pregnancy test are positive.
• What are the causes of syncope?
The causes of syncope are varied, ranging from benign to
life-threatening. Syncope can best be classified as cardiac or
noncardiac in etiology (Table 2). Despite thorough evaluation, 30% to 50% of syncope cases seen in the ED are of unexplained etiology [4,11].
Noncardiac Causes
The most commonly identified etiology of syncope is vasovagal or neurocardiogenic syncope. Vasovagal syncope is characterized by a prodrome lasting more than 5 seconds [12,13]
www.turner-white.com
CASE-BASED REVIEW
and is associated with precipitating events or stresses [13,14].
Common stresses include unexpected pain, fear, unpleasant
sight, sound or smell, and prolonged standing at attention.
Situational syncope is also vagally mediated and is characterized by episodes occurring during or immediately after micturition, defecation, cough, or swallowing [15]. Carotid-sinus
syncope is another variety of neurally mediated or vasovagal
syncope.
Hypovolemia due to dehydration, medication, or hemorrhaging is another common cause of syncope [9]. A hypovolemic etiology of syncope is often manifested as orthostatic hypotension, which is defined as a decrease in systolic
blood pressure of 20 mm Hg or greater or an increase in
heart rate of 15 bpm within 2 minutes of standing. In contrast, general tachycardia or hypotension is nonspecific for
hemodynamic instability or volume depletion. The presence
of orthostatic hypotension can therefore aid in correctly
attributing a syncopal episode to volume depletion, autonomic insufficiency, or medications. Orthostatic hypotension
is commonly seen in patients who suffer from recurring
episodes of syncope or lightheadedness and is a common
finding in pregnancy. Orthostatic hypotension is present in
up to 40% of asymptomatic patients older than 70 years and
23% of patients who are younger than 60 years [16].
Medications causing syncope include most antihypertensive and cardiovascular agents, such as diuretics and vasodilators. Drugs that prolong the QT interval are associated
with life-threatening arrhythmias. The geriatric patient taking multiple medications is especially at risk for medicationinduced syncope [17].
Generalized anxiety and panic disorders as well as major
depression have been associated with vasovagal syncope
[18]. Fainting is a known manifestation of somatization disorder [18].
Cardiac Causes
Cardiac syncope is characterized by an absent or brief prodrome (less than 5 seconds), palpitations, and brief loss of
consciousness. Cardiac syncope often occurs while the patient is seated or reclining; however, neurologic syncope also
may occur in the seated or reclined position [13].
Syncope of cardiac etiology can be classified into mechanical or obstructive causes and dysrhythmic or electrical causes. These range from aortic stenosis and cardiac tamponade
to paroxysmal ventricular tachycardia and a conduction system disease. These types of underlying medical conditions
are more easily diagnosed in the presence of associated respiratory or neurologic symptoms or chest pain. A patient
with a history of cardiac disease will likely have a cardiac
cause of syncope. A history of ventricular arrhythmia or congestive heart failure is predictive for an adverse outcome
[2,7,11]. Patients who experience cardiac syncope and who
www.turner-white.com
Table 2. Etiology of Syncope
Vasovagal/neurocardiogenic
Hypovolemic
Dehydration
Medication
Hemorrhage
Hypoglycemia
Psychiatric
Cardiac
Dysrhythmic or electrical
Mechanical or obstructive
Unexplained syncope
also have poor left ventricular function have a higher risk of
sudden death [19,20].
Syncope following exertion may indicate structural heart
disease, such as with obstruction of left ventricular outflow
due to fixed (aortic stenosis) or dynamic (hypertrophic cardiomyopathy) causes [21]. Young patients who present with
syncope following exercise and who have a family history of
syncope, sudden death, or arrhythmias should be scrupulously evaluated for a cardiac etiology [22]. Careful attention
should be paid to prolonged QT intervals or evidence of
hypertrophic cardiomyopathy [22].
• Does diagnosis of syncope differ by age-group?
In patients younger than 65 years, noncardiac causes make
up approximately 40% of syncope cases, while 20% may be
attributed to cardiac abnormalities. In those aged 65 years or
older, cardiac causes comprise up to 40% of cases, while noncardiac causes comprise only 20% [23]. In general, syncope
in children and adolescents is a benign event. However, syncope that occurs during exercise can be indicative of a potentially fatal condition [16,22]. In younger individuals, syncope
is most often associated with a single, isolated disease process [24,25].
Women and individuals younger than 55 years of age are
more likely to experience neurally mediated hypotension.
These episodes often last longer than 5 seconds and occur
while the person is standing or emotionally upset. Symptoms that accompany this form of syncope include palpitations, blurred vision, and nausea [15]. Frequently recurring
syncope in young patients with no heart disease may be due
to psychiatric disorders [18].
Syncope in elderly patients is more difficult to diagnose
and is associated with a higher level of morbidity and mortality, particularly due to trauma associated with falls following
Vol. 10, No. 1 January 2003 JCOM 41
SYNCOPE
Table 3. Approach to Diagnostic Testing in Syncope
Likely arrhythmic cause:
Consider electrophysiologic
testing
Serial cardiac enzymes
Cardiac-associated chest pain
or ECG signs of ischemia:
Valvular disease by physicial exam: Echocardiography
Possible cardiac etiology:
Holter or continuous-loop
monitoring
Unexplained recurrent syncope:
Consider tilt-table testing
Unexplained syncope in patient
Carotid sinus massage
older than age 40 years:
Women of childbearing age:
Pregnancy test
Possible neurologic etiology:
Head CT and EEG
Possible psychiatric etiology:
Psychiatric evaluation
CT = computed tomography; ECG = electrocardiogram; EEG = electroencephalogram.
syncopal events [26]. The causes of syncope are more complex
and often multifactorial in the elderly [24,25]. The elderly
often have numerous medical conditions, requiring multiple
medications, many of which can cause syncope. Furthermore,
age alone predisposes to syncope, as many of the physiologic
changes associated with the aging process result in decreased
cerebral perfusion [25]. As one ages, there is a decrease in the
body’s ability to respond to hypotensive challenges and syncope can commonly ensue[3].
• What diagnostic measures should be considered in
evaluating the syncope patient?
The history and the physical examination identify a cause of
syncope in 45% of patients [27]. While the diagnostic yield of
an ECG in syncope is only 5% [7,26], a standard 12-lead ECG
should be used for patients in whom there is a possibility of
cardiac disease to help identify myocardial infarction or lifethreatening dysrhythmias. Martin et al found that an abnormal ECG is a multivariate predictor for arrhythmia or death
for 1 year following an episode of syncope [28]. An ECG may
also aid in identifying prolonged QT intervals as the cause of
the syncope [29].
In patients in whom a diagnosis cannot be made after history, physical examination, and ECG, targeted diagnostic
testing should be undertaken (Table 3). In syncope, there is
no gold standard against which the results of diagnostic tests
can be measured. Hence, it remains difficult to ascertain sensitivity and specificity of these tests [27,30].
If the presence of a significant arrhythmia is suspected,
prolonged cardiac monitoring of up to 72 hours may be
warranted. This includes patients who are male, older than
42 JCOM January 2003 Vol. 10, No. 1
65 years, have a history of heart disease, and have an abnormal rhythm on initial ECG. However, many arrhythmias
discovered in a 24- to 72-hour window of monitoring are
asymptomatic [31]. Holter monitoring in patients with syncope suggestive of a cardiac cause or in patients with unexplained syncope may demonstrate symptoms in conjunction with arrhythmias in 4% of patients and symptoms
without arrhythmias in 17% [32]. In utilizing continuousloop recorders in patients with frequently recurring syncope, arrhythmias were foundduring syncope in 8% to 20%,
and normal rhythm was found during symptoms in 12% to
27% [33]. Implantable subcutaneous continuous-loop
recorders may increase the yield slightly [34]. The diagnostic yield of longer-term monitoring is higher and thus its
utilization is justified predicated on the clinical suspicion of
an arrhythmia as the etiology of a syncopal event. Longerterm monitoring may also be of benefit in patients with
recurrent syncope of unknown etiology.
History, physical examination, and ECG are often sufficient
to identify the presence of heart disease [9]. Only when the
presence or absence of underlying cardiac disease cannot be
determined clinically is an echocardiogram helpful as echocardiograms rarely reveal unsuspected abnormalities and generally do not lead to the diagnosis ofa cause [35].
The European Society of Cardiology recommends carotid
sinus massage in patients older than 40 years with syncope of
unknown etiology, and it also should be considered in patients with spontaneous symptomssuggestive of carotid sinus
syncope, such as syncope while shaving or while turning the
head [36]. However, in patients with a history of carotid artery
disease, this maneuver should be avoided.
Passive upright tilt-table testing at 60 degrees for 45 minutes may be appropriate in patients with unexplained recurrent syncope in whom cardiac causes of syncope, including
arrhythmias, have been excluded [30]. In patients with negative results on a passive tilt-table test who have a high
pretest probability of neurally mediated syncope, such as
young patients with a prodrome of nausea or warmth, tilttable testing with isoproterenol is recommended. The test
results should be considered positive only if a patient’s typical symptoms are reproduced [30].
Electrophysiologic testing is indicated when initial evaluation suggests an arrhythmic cause of syncope, such as patients with abnormal ECG and/or structural heart disease,
palpitations, or family history of sudden death [27,35]. Electrophysiologic testing may be helpful in guiding therapy
in patients with syncope and a high-risk profession such
as airline pilots [36]. Single-averaged ECG is not diagnostic
of the cause of syncope but may be useful in selecting
patients for electrophysiologic studies when coronary artery
disease is present and ventricular tachycardia is suspected
[30,36].
www.turner-white.com
CASE-BASED REVIEW
Neurologic testing is useful only in patients who have
focal neurologic findings or a history consistent with a
seizure [27,36]. An electroencephalogram provides diagnostic information in less than 2% of cases of syncope [37].
Computed tomography scans of the head providenew diagnostic information in 4% of cases [38]. Psychiatric evaluation
should be considered in patients with known psychiatric illness, no organic heart disease, and recurrent syncope [9].
Blood tests are commonly ordered but are often unnecessary since they do not yield diagnostically useful information [7,12,39]. In patients in whom seizure rather than syncope is suspected, serum glucose and bicarbonate levels may
be helpful [6]. If blood loss is suspected, examination for the
presence of blood in the stool may be more useful than
checking hematocrit or hemoglobin since they may be normal in early stages of blood loss [40]. In addition, a pregnancy test should be considered in women of childbearing age
who experience syncope. However, a physician should not
mechanically interpret a pregnancy as the sole cause of a
syncopal episode. Rather, a complete evaluation of the patient should be done to fully identify the etiology [41].
• Which patients with syncope should be admitted to the
hospital?
The cost of care per hospital admission for syncope has been
estimated at approximately $5300 per stay for a total cost of
over $1 billion per year nationally [1,38]. Although in current practice there is a liberal policy toward hospital admission, no study proves that hospital admission improves
outcome for patients with syncope of undetermined etiology [41]. The American College of Emergency Physicians recommends admitting syncope patients with any of the following [41]:
1. A history of congestive heart failure or ventricular
arrhythmias
2. Associated chest pain or other symptoms compatible with acute coronary syndrome
3. Evidence of significant congestive heart failure or
valvular heart disease on physical examination
4. ECG findings of ischemia, arrhythmia, prolonged
QT interval, or bundle branch block
In addition, admission should be considered for patients who
are older than 60 years, have a history of coronary heart disease or congenital heart disease, or have a family history of
sudden death [41]. These recommendations have been tested
and validated in a recent prospective trial [42].
www.turner-white.com
Further Testing and Diagnosis
Despite the positive pregnancy test, which may indicate a benign etiology of syncope, the ED physician decides to admit the patient based on a concern for
valvular heart disease. The patient undergoes an echocardiogram, and the presence of a bicuspid aortic valve and
mild aortic stenosis is noted. The patient is informed that the
murmur is congenital and, given the current mild nature of
her aortic stenosis, there is no immediate cause for concern.
Nevertheless, she will need to be followed closely by a cardiologist for serial heart examinations and echocardiography. Additionally, the patient is told that the syncopal episode can be explained by increased demands of cardiac
output due to her pregnancy. Physiologic changes during
pregnancy affect hemodynamic balance controlled by blood
volume and myocardial contractility and therefore may
make the patient more prone to syncope [43].
• What are the outcomes of syncope patients?
Despite established guidelines on management of syncope,
there is little available medical literature discussing shortterm outcomes of syncope patients following discharge from
the ED. Most literature has studied outcomes of patients at
6-month and 1-year intervals. However, one study determined 4 predictors of adverse outcomes at 72 hours. These
factors include a history of ventricular arrhythmias, an abnormal ECG in the ED, age greater than 45 years, and a history of congestive heart failure [44]. In patients with none of
these risk factors, there was no risk of cardiac mortality but
a 0.7% risk of an arrhythmia [44].
Martin identified predictors of arrhythmias within 1 year
of presentation of the syncope patient to the ED; these included age greater than 45 years, male sex, and nonwhite race
[28]. In patients with 3 or more of these risk factors, there was
at least a 57.6% risk of 1-year all-cause mortality or significant
arrhythmia [28]. Other studies have shown that patients
older than 60 years as well as patients of any age having a cardiovascular diagnosis have an increase in sudden death within 2 years [41].
The San Francisco Syncope Rule may be helpful as a
means of predicting patients with serious outcomes at 1 week.
Supporting data suggest that age greater than 75 years, an
abnormal ECG, hematocrit less than 30, a complaint of shortness of breath, and a history of CHF are all significant risk factors for poor outcome at 1 week [45].
The 1-year mortality differs in patients with cardiac syncope versus noncardiac or unexplained syncope. Cardiac
syncope patients have 18% to 33% mortality in contrast to
3% to 4% in noncardiac or unexplained syncope [23]. In
Vol. 10, No. 1 January 2003 JCOM 43
SYNCOPE
addition, cardiac syncope is an independent predictor of
mortality when taking into account baseline cardiac conditions such as past congestive heart failure or myocardial
infarction [38].
One prospective cohort study showed that patients older
than 60 years and those with a cardiovascular diagnosis
regardless of age had an increase in sudden death within
2 years. The study also found that the elderly were more likely to have severe trauma from falls related to syncope [25].
There have been additional studies that have correlated
short-term mortality after a syncopal episode with advanced
age [3,4]. Thirty percent of non-institutionalized elderly patients over age 75 years will experience a repeat syncopal
episode within 2 years [38].
Summary
Despite increasing emphasis on evidence-based medicine,
efforts to reduce unnecessary and expensive medical testing,
and concerns over the rapidly rising costs of medical care,
syncope remains a frequent cause for medical admission and
expensive clinical workup. More often than not no definitive
diagnosis or intervention is made. Further studies focusing
on outcome of patients with syncope will be helpful in future
management of these patients in the ED setting. Ultimately,
the role of the physician in distinguishing potentially lifethreatening causes of syncope from benign ones is crucial in
assuring the well-being of these patients.
Corresponding author: Shamai A. Grossman, MD, MS, Dept. of
Emergency Medicine, Beth Israel Deaconess Medical Center, One
Deaconess Rd., West Clinical Center 2, Boston, MA 02215, sgrossma@
caregroup.harvard.edu.
Financial disclosures: None.
Author contributions: conception and design, SAG, RK; drafting of
the article, SAG, RK; critical revision of the article, SAG, RK; final
approval of the article, SAG, RK.
References
1. Lipsitz LA. Syncope in the elderly. Ann Intern Med 1983;99:
92–105.
2. Kapoor W, Snustad D, Peterson J, et al. Syncope in the elderly. Am J Med 1986;80:419–28.
3. Lipsitz LA, Pluchino FC, Wei JY, Rowe JW. Syncope in institutionalized elderly: the impact of multiple pathological conditions and situational stress. J Chronic Dis 1986;39:619–30.
4. Getchell WS, Larsen GC, Morris CD, McAnulty JH. Epidemiology of syncope in hospitalized patients. J Gen Intern
Med 1999;14:677–87.
5. Ooi WL, Hossain M, Lipsitz LA. The association between
orthostatic hypotension and recurrent falls in nursing home
residents. Am J Med 2000:108;106–11.
6. Harwood-Nuss AL. The clinical practice of emergency med44 JCOM January 2003 Vol. 10, No. 1
icine. 2nd edition. Philadelphia: Lippincott-Raven; 1996.
7. Kapoor WN, Karpf M, Wieand S, et al. A prospective evaluation and follow-up of patients with syncope. N Engl J Med
1983;309:197–204.
8. Marx JA, Hockerberger RS, Walls RM, Adams J. Rosen’s
emergency medicine: concepts and clinical practice. 5th edition. St. Louis (MO): Mosby; 2002.
9. Kapoor WN. Syncope. N Engl J Med 2000;343:1856–62.
10. Benbadis S, Wolgamuth B, Goren H, et al. Value of tongue
biting in the diagnosis of seizures. Arch Intern Med 1995;
155:2346–9.
11. Kapoor WN, Hanusa BH. Is syncope a risk factor for poor
outcomes? Comparison of patients with and without syncope. Am J Med 1996;100:646–55.
12. Martin GJ, Adams SL, Martin HG, et al. Prospective evaluation of syncope. Ann Emerg Med 1984;13:499–504.
13. Calkins H, Shyr Y, Frumin H, et al. The value of the clinical
history in the differentiation of syncope due to ventricular
tachycardia, atrioventricular block, and neurocardiogenic
syncope. Am J Med 1995;98:365–73.
14. Day SC, Cook EF, Funkenstein H, Goldman L. Evaluation
and outcome of emergency room patients with transient loss
of consciousness. Am J Med 1982;73:15–23.
15. Braunwald E, editor. Heart disease: a textbook of cardiovascular medicine. 5th edition. Philadelphia: Saunders; 1997.
16. Atkins D, Hanusa B, Sefcik T, Kapoor W. Syncope and orthostatic hypotension. Am J Med 1991;91:179–85.
17. Hanlon JT, Linzer M, MacMillan JP, et al. Syncope and presyncope associated with probable adverse drug reactions.
Arch Intern Med 1990;150:2309–12.
18. Kapoor WN, Fortunato M, Hanusa BH, Schulberg HC. Psychiatric illnesses in patients with syncope. Am J Med 1995;99:
505–12.
19. Middlekauff HR, Stevenson WG, Saxon LA. Prognosis after
syncope: impact of left ventricular function. Am Heart J 1993;
125:121–7.
20. Middlekauff HR, Stevenson WG, Stevenson LW, Saxon LA.
Syncope in advanced heart failure: high risk of sudden death
regardless of origin of syncope. J Am Coll Cardiol 1993;21:
110–6.
21. Manolis AS. The clinical spectrum and diagnosis of syncope.
Herz 1993;18:143–54.
22. Driscoll DJ, Jacobsen SJ, Porter CJ, Wollan PC. Syncope in
children and adolescents. J Am Coll Cardiol 1997;29:1039–45.
23. Kapoor WN. Evaluation and management of the patient
with syncope. JAMA 1992;268:2553–60.
24. Besdine RW. Geriatric medicine. An overview. Annu Rev
Gerontol 1980;1:135–53.
25. Kapoor WN. Evaluation of syncope in the elderly. J Am
Geriatr Soc 1987;35:826–8.
26. Kapoor WN. Diagnostic evaluation of syncope. Am J Med
1991;90:91–106.
27. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope.
Part 1. Value of history, physical examination, and electrocardiography: Clinical Efficacy Assessment Project of the American College of Physicians. Ann Intern Med 1997;126:989–96.
28. Martin TP, Hanusa BH, Kapoor WN. Risk stratification of
www.turner-white.com
CASE-BASED REVIEW
patients with syncope. Ann Emerg Med 1997;29:459–66.
29. Klitzner TS. Sudden cardiac death in children. Circulation
1990;82:629–32.
30. Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing syncope.
Part 2. Unexplained syncope: Clinical Efficacy Assessment
Project of the American College of Physicians. Ann Intern
Med 1997;127:76–86.
31. Bass EB, Curtiss EI, Arena VC, et al. The duration of Holter
monitoring in patients with syncope. Is 24 hours enough?
Arch Intern Med 1990;150:1073–8.
32. DiMarco JP, Philbrick JT. Use of ambulatory electrocardiographic (Holter) monitoring. Ann Intern Med 1990;113:
53–68.
33. Linzer M, Pritchett EL, Pontinen M, et al. Incremental diagnostic yield of loop electrocardiographic recorders in unexplained syncope. Am J Cardiol 1990;66:214–9.
34. Krahn AD, Klein GJ, Yee R, et al. Use of an extended monitoring strategy in patients with problematic syncope. Circulation 1999;99:406–10.
35. Recchia D, Barzilai B. Echocardiography in the evaluation of
patients with syncope. J Gen Intern Med 1995;10:649–55.
36. Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope. Eur Heart J
2001;22:1256–306.
37. Davis TL, Freemon FR. Electroencephalography should not
be routine in the evaluation of syncope in adults. Arch Intern
Med 1990;150:2027–9.
38. Kapoor WN. Evaluation and outcome of patients with syncope. Medicine 1990;69:160–75.
39. Eagle KA, Black HR. The impact of diagnostic tests in evaluating patients with syncope. Yale J Biol Med 1983;56:1–8.
40. Shotan A, Ostrzega E, Mehra A, et al. Incidence of arrhythmias in normal pregnancy and relation to palpitations, dizziness, and syncope. Am J Cardiol 1997;79:1061–4.
41. American College of Emergency Physicians. Clinical policy:
critical issues in the evaluation and management of patients
presenting with syncope. Ann Emerg Med 2001;37:771–6.
42. Elesber AA, Decker WW, Smars PA, et al. Evaluation of the
safety and cost-effectiveness of the ACEP clinical policy in
regards to admission of the syncopal patient. Acad Emerg
Med 2002;9:370–1.
43. Gei AF, Hankins GD. Cardiac disease and pregnancy. Obstet
Gynecol Clin North Am 2001;28:465–512.
44. Gallagher EJ. Hospitalization for fainting: high stakes, low
yield. Ann Emerg Med 1997;29:540–2.
45. Quinn IG, Stiell IG, Seller KA, et al. The San Francisco syncope rule to predict patients with serious outcomes. Acad
Emerg Med 2002;9:358.
Copyright 2003 by Turner White Communications Inc., Wayne, PA. All rights reserved.
www.turner-white.com
Vol. 10, No. 1 January 2003 JCOM 45
JCOM
CME
EVALUATION FORM: Syncope: Diagnosis and Evidence-Based Management
To receive 1 hour of AMA PRA Category 1 CME credit, read the article named above and mark your responses on this form. You
must complete all parts to receive credit. Then return this form using the fax number or address appearing at the bottom of this
page. A certificate awarding 1 hour of category 1 CME credit will be sent to you by fax or mail. This CME Evaluation Form must
be fax marked or postmarked within 1 year of this JCOM issue date. Please allow up to 4 weeks for your certificate to arrive.
Part 1. Please respond to each statement.
Strongly Agree
Strongly Disagree
5
4
3
2
1
I was provided with new information pertinent to my practice.
❏
❏
❏
❏
❏
I reaffirmed a specific skill or knowledge.
❏
❏
❏
❏
❏
This article will help with clinical decision making.
❏
❏
❏
❏
❏
Relevant clinical outcomes are addressed.
❏
❏
❏
❏
❏
The case is communicated in a manner that kept my interest.
❏
❏
❏
❏
❏
The case presentation is realistic and effective.
❏
❏
❏
❏
❏
I could easily interpret the tables and figures.
❏
❏
❏
❏
❏
My attitude about this topic changed in some way.
❏
❏
❏
❏
❏
Additional comments: ______________________________________________________________________________________
__________________________________________________________________________________________________________
Part 2. Please complete the following sentence.
As a result of reading this case study, I . . .
❏ see no need to change my practice.
❏ will seek more information before modifying my practice.
❏ intend to change the following aspect(s) of my practice: (Briefly describe)
__________________________________________________________________________________________________________
__________________________________________________________________________________________________________
Part 3. Statement of completion: I attest to having completed the CME activity.
Signature: _________________________________________ Date: _________________________________________________
Part 4. Identifying information: Please PRINT legibly or type the following:
Name: ____________________________________________ Fax number ___________________________________________
Address: __________________________________________ Telephone number ______________________________________
__________________________________________________ Social Security number: __________________________________
(Required and confidential)
__________________________________________________
Medical specialty: __________________________________
Wayne State University School of Medicine is accredited by the Accreditation Council for Continuing
Medical Education to provide continuing medical eduSEND THE COMPLETED
cation for physicians.
CME EVALUATION FORM TO:
Wayne State University School of Medicine desigBY FAX: 313-577-7554
nates this CME activity for a maximum of 1 hour of catBY MAIL: Wayne State University
egory 1 credit toward the Physician’s Recognition
Division of CME
Award of the American Medical Association. Physicians
should claim only those hours of credit actually spent in
101 Alexandrine, Lower Level
the educational activity.
Detroit, MI 48201
46 JCOM January 2003 Vol. 10, No. 1
www.turner-white.com