CHAPTER 6
Content
GENERA LPRINCIPLES
•
The evaluation of syncope can be daunting as there are a myriad of
circumstances that can cause or mimic this common clinical problem.
• It is a presentation that requires a consistent approach with realization that
we often will never know with certainty the original precipitating etiology.
• Our role as consultants is to help risk stratify these patients for future events
via diagnostic testing, as appropriate, and to recommend therapy to
prevent recurrences and reduce the risk of injury or death.
Def in itio n
• The term “syncope” should be applied to situations where there is
Temporary, transient loss of consciousness
(TLOC) Complete and, typically, rapid recovery
Global cerebral hypoperfusion as the final common pathway regardless
of etiology
• Otherwise, the episode should be referred to as “TLOC” so as to include
nonsyncopal etiologies in the differential diagnosis (Table 6-1).
Epidemio l o gy
• The lifetime incidence of syncope is 30% to 50%.1-3
• It accounts for 3% to 5% of emergency room visits and 1% to 6% of
hospital admissions. Many more cases of syncope are not reported.4
• Large population data showed a rate of 6.2 per 1,000 person-years, with
an
increasing incidence in the elderly. 5 For institutionalized patients over the age
of
70, the incidence is as high as 23% over 10 years.6
Etio l o gy
• Syncope first must be differentiated from nonsyncopal events involving real
or apparent TLOC, such as seizures and falls (Table 6-1).
• Further subdivision of true syncope is based on specific
pathophysiologic etiologies that include the following four general categories
(Table 6-2) in descending order of frequency:
Neurally mediated (reflex) syncope
Orthostatic syncope
Primary cardiac arrhythmias
Structural cardiac or cardiopulmonary disease
DIA GNO SIS
Cl in ic al Pr esen tatio n
• Initial evaluation of syncope utilizes the history, physical examination, and
electrocardiogram (ECG) to classify presumed causes and identify patients
who are at high risk for death. There are three key questions that need to be
answered with the initial evaluation:
86
Is loss of consciousness attributable to syncope or
not? Is heart disease present or not?
Are there important clinical features in the history that suggest the diagnosis?
• In addition, consideration of inpatient versus outpatient evaluation should
depend on comorbidities and initial findings. In general, patients with the
following should be admitted to avoid delay and adverse outcomes:
Elderly (age > 65 years)
Known structural heart
disease
Symptoms suggestive of primary cardiac syncope
Abnormal ECG
Severe orthostatic hypotension
Focal neurological deficits
87
87
Family history of sudden death
Exertional syncope
Syncope causing severe injury
Syncope while driving
Histo ry
• Often, the diagnosis of syncope is evident from the history.
• Aspects of the history that need to be explored in order to aid diagnosis
and further categorize the event include a prodrome before the attack,
eyewitness accounts during the event, the patient’s recollection immediately
after the attack, circumstances that may have played a causative role in the
event, and general questions about the patient’s medical history.
• A helpful mnemonic is, “I passed out on the BEACH” (Table 6-3).
• For patients with recognizable reflex or orthostatic syncope that
occurs infrequently or as an isolated episode, no further workup is
necessary. These patients generally have a good prognosis and can be managed
as outpatients with treatments listed below.
• In patients with a suspected cardiac etiology, an inpatient cardiac
evaluation is warranted.
Ph ysical Examin atio n
• The examination should include assessment of orthostatic vital signs and
careful neurologic, pulmonary, and cardiovascular assessment.
Proper orthostatic vital signs
include
Blood pressure (BP) checked (both arms) after the patient lies supine for
at least 5 minutes
BP measured 3 minutes after standing
Orthostasis = 20-mmHg decrease in systolic BP and/or 10-mmHg decrease
in diastolic BP and/or 10-bpm increase in heart rate (HR)
Cardiovascular findings that may point to cardiogenic syncope
include
Arrhythmias (tachyarrhythmias, bradyarrhythmias, and irregularity)
Murmurs (especially aortic stenosis or hypertrophic
obstructive cardiomyopathy)
Evidence for heart failure (S3, S4, edema, and elevated JVD)
Neurologic findings are often absent, but might include evidence of
autonomic neuropathy (e.g., inappropriate sweating, lack of HR variability,
extreme orthostatic BP changes).
A firm massage at the carotid artery bifurcation for 5 to 10 seconds
may reproduce symptoms, particularly in the elderly.
This maneuver can be performed safely at the bedside with the patient lying
recumbent on telemetry monitoring and appropriate bradycardia treatments
available.
The test is considered positive if it results in a ventricular pause of
>3 seconds.
Neurologic complications are rare (<0.5%), but the procedure should
be avoided in patients with known carotid disease, carotid bruits, or a
recent transient ischemic attack (TIA)/cerebrovascular accident.
Diagn o stic Testin g
• Given the broad differential, the syncope evaluation is notorious for
triggering extensive, multimodality diagnostic testing.
• The 2006 American Heart Association (AHA)/American College of
Cardiology
(ACC) algorithm for cardiac evaluation of syncope is outlined in Figure 6-1.7
El ectro cardio graph y
Specific abnormalities to look for on ECG include
• Evidence of sinus node dysfunction
• Evidence of atrioventricular conduction abnormalities
• Tachyarrhythmias (supraventricular tachycardia [SVT], ventricular
tachycardia
[VT], atrial fibrillation [AF])
• Evidence of ventricular preexcitation (delta waves)
• Evidence of underlying structural heart disease
includes Q waves suggestive of prior myocardial
infection Wide QRS (>120 milliseconds)
Left ventricular hypertrophy pattern suggestive of hypertrophic
cardiomyopathy
(HCM)
Anterior precordial T-wave inversions and/or epsilon waves suggestive
of arrhythmogenic right ventricular dysplasia (ARVD)
• Evidence of
channelopathy: Long or
short QT.
Right bundle branch block with down-sloping ST elevation and T-wave
inversion in V1–V3 (Brugada pattern).
Imagin g
•
The expanded cardiac evaluation includes an echocardiogram, exercise
testing, and an ischemic evaluation.
In appropriate patients, an exercise stress echo would be sufficient to
complete
all three aspects of testing (baseline imaging followed by exercise protocol
and stress imaging).
The echocardiogram alone may be diagnostic in cases of valvular heart
disease, cardiomyopathy, or congenital heart disease.
Exercise testing is preferable to pharmacologic stress and should be
symptom- limited.
Noninvasive
testing
for
ischemia
should
be
followed
by
cardiac catheterization if there is an evidence of ischemia or previously
unrecognized infarction.
• Cardiac magnetic resonance imaging or computed tomography may be helpful
in
the evaluation of structural heart disease, including HCM, ARVD, or
coronary anomalies.
• If an arrhythmic cause is suspected, but not evident on the initial workup or
on expanded cardiac evaluation, ambulatory cardiac rhythm monitoring
can be achieved via one of the following modalities8:
Holter monitor (24 to 48 hours of continuous
recording)
Event recorder (1 month of patient-activated or patient-triggered recordings to
temporally correlate with symptoms)
90
90
Mobile Continuous Outpatient Telemetry (MCOT) for up to one month of
continuous monitoring
Implantable loop recorder (years of continuous
recording)
91
91
FIGU RE 6- 1 . Al go rith m fo r th e eval uatio n o f syn co pe. (Mo dified fro m American Heart Asso ciatio n
/American Co l l ege o f
Cardio l o gy Fo un datio n . AHA/ACCF scien tific statemen to n th e eval uatio n o f syn co pe. Circul atio n 2006;113:316.)
The choice of monitoring is dependent on the frequency of symptoms and type
of suspected arrhythmia. Even in a highly selected population, the diagnostic
yield of ambulatory cardiac monitoring is relatively low.
• Tilt table testing has been used traditionally as a diagnostic tool to characterize
a patient’s hemodynamic response to controlled postural change from
supine to upright state to aid in the diagnosis of a reflex-mediated
(neurocardiogenic) syncope.
Physiologically, there is a large volume shift during repositioning, with 500
to
1000 mL of blood moving from the thorax to the distensible venous system
below the diaphragm within the first 10 seconds.
The hydrostatic pressures created by the upright position result in a
similar volume of fluid moving to the interstitial space within 10 minutes.
Autonomic vasoconstriction is the key reflex to counter this orthostatic
stress, and failure of the vasoconstriction mechanism at any point may
result in syncope.
An under-filled right ventricle will trigger a strong vagal response, leading
to bradycardia and hypotension
Results are classified as primarily vasodepressor, cardioinhibitory, or mixed.
Unfortunately, the test has a low sensitivity and reproducibility. It is
our institutional bias that a tilt table test adds very little to a thorough
history, physical examination, and standard cardiac workup of syncope.
• Electrophysiology studies (EPS) can be useful in selected patients.
Indications for EPS include
Abnormal ECG suggesting conduction system cause
Syncope during exertion or while supine or in the presence of structural
heart disease
Syncope with associated palpitations
Family history of sudden death
To define/ablate identified arrhythmias in patients with high-risk occupations
TREA TMENT
• Treatment of syncope can be broadly defined as preventing recurrences
and
reducing the risk of injury or death.
• In general, this is tailored to treat the suspected underlying etiology of the
syncope.
• Various approaches to treating the four etiologies of syncope are shown in
Table
6-4.
Medic atio n s
• The most common pharmacologic options for preventing venous pooling
and aiding intravascular volume expansion include
Midodrine (2.5 to 10 mg by mouth (PO) three times a day)9,10
Peripheral α-agonist causing both arterial and venous constriction
Adverse effects: paresthesias, piloerection, pruritus, and supine
hypertension Avoid in patients with carotid artery disease (CAD),
peripheral arterial disease, and acute renal failure
The only drug shown effective in trials for orthostatic hypotension and
reflex- mediated syncope
Fludrocortisone (start 0.1 mg PO daily, can increase by 0.1 mg weekly
to
maximum of 1.0 mg PO daily)
Synthetic mineralocorticoid causing sodium retention and volume expansion
Adverse effects: hypertension, peripheral edema, and hypokalemia11
An ongoing randomized control trial (POST II) is investigating
effectiveness in reflex syncope12
β-Blockers are often prescribed for syncope, though trials do not support
this
practice.13
O th er No n ph ar mac o l o gic Th er apies
• For reflex syncope, effective treatment may be as simple as avoiding
syncopal precipitants.
• When such precipitants cannot be avoided, coping strategies can be
helpful.
Isometric muscle contractions can improve venous return and abort frank
syncope in patients with a recognizable prodrome.
Lif estyl e/ Risk Mo dif ic atio n
• Driving restrictions should be discussed in patients with unexplained
syncope when appropriate.
• Recommendations currently vary depending on etiology, underlying disease,
type of license held (private versus commercial), and adequacy of treatment.
• If cause of syncope is an active cardiac arrhythmia, patients should be
instructed not to drive until successful treatment has been initiated and the
patient has received permission from the treating physician.
• In general, in patients with a serious episode of syncope that is not clearly due to
a reversible etiology, guidelines recommend driving restriction for 3 to 6
syncope- free months. Also, federal law and variable state law pertinent to
licensure in these individuals exist and should be consulted when applicable.
O UTCO ME/ PRO GNO SIS
• One-third of the patients with syncope will have a recurrent event within 3 years.
• Select subgroups of patients with noncardiac syncope who have an
excellent prognosis. Young, otherwise healthy individuals with a normal ECG
and without identifiable heart disease have essentially no increased risk of death
relative to the population at large.
• Reflex syncope is associated with no increase in mortality risk.
• Syncope from orthostatic hypotension has an excellent prognosis if the
underlying abnormality is easily identified and treated.
• In contrast, syncope with an identifiable cardiac etiology carries a higher risk
of mortality, particularly in patients with advanced heart failure. Mortality
approaches 45% at 1 year for patients with syncope and left ventricular (LV)
ejection fraction <20%.14
REFERENCES
1. Kenny RA, Bhangu J, King-Kallimanis BL. Epidemiology of syncope/collapse in younger and older
Western patient populations. Prog Cardiovasc Dis 2013;55:357-363.
2. Ganzeboom KS, Mairuhu G, Reitsma JB, et al. Lifetime cumulative incidence of syncope in the
general population: a study of 549 Dutch subjects aged 35-60 years. J Cariovasc Electrophysiol
2006;17:1172-1176.
3. Manolis AS, Linzer M, Salem D, Estes NA, 3rd. Syncope: current diagnostic evaluation and
management.
Ann Intern Med 1990;112:850-863.
4. Shen WK, Decker WW, Smars PA, et al. Syncope Evaluation in the Emergency Department Study
(SEEDS):
a multidisciplinary approach to syncope management. Circulation 2004;110: 3636-3645.
5. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J
Med
2002;347:878-885.
6. Lipsitz LA, Wei JY, Rowe JW. Syncope in an elderly, institutionalised population. prevalence, incidence,
and associated risk. Q J Med 1985;55:45-54.
7. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF Scientific Statement on the evaluation
of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular
Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes
Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in
collaboration with
the Heart Rhythm Society: endorsed by the American Autonomic Society. Circulation
2006;113:316-327.
8. Subbiah R, Gula LJ, Klein GJ, et al. Syncope: review of monitoring modalities. Curr
Cardiol Rev 2008;4:4148.
9. Low PA, Gilden JL, Freeman R, et al. Efficacy of midodrine vs placebo in neurogenic
orthostatic hypotension.
A randomized, double-blind multicenter study. Midodrine Study Group. JAMA 1997;277:10461051.
10. Wright RA, Kaufmann HC, Perera R, et al. A double-blind, dose-response study of
midodrine in neurogenic orthostatic hypotension. Neurology 1998;51:120-124.
11. Chobanian AV, Volicer L, Tifft CP, et al. Mineralocorticoid-induced hypertension in
patients with orthostatic hypotension. N Engl J Med 1979;301:68-73.
12. Raj SR, Rose S, Ritchie D, et al.; POST II Investigators. The Second Prevention of Syncope
Trial (POST II)
—a randomized clinical trial of fludrocortisone for the prevention of neurally mediated
syncope: rationale and study design. Am Heart J 2006;151:1186.e11-17.
13. Sheldon R, Connolly S, Rose, et al. POST Investigators. Prevention of Syncope Trial
(POST): a randomized, placebo-controlled study of metoprolol in the prevention of
vasovagal syncope. Circulation 2006;113:11641170.
14. Middlekauff HR, Stevenson WG, Stevenson LW, et al. Syncope in advanced heart failure:
high risk of sudden death regardless of origin of syncope. J Am Coll Cardiol 1993;21:110116.
•
The evaluation of syncope can be daunting as there are a myriad of
circumstances that can cause or mimic this common clinical problem.
• It is a presentation that requires a consistent approach with realization that
we often will never know with certainty the original precipitating etiology.
• Our role as consultants is to help risk stratify these patients for future events
via diagnostic testing, as appropriate, and to recommend therapy to
prevent recurrences and reduce the risk of injury or death.
Def in itio n
• The term “syncope” should be applied to situations where there is
Temporary, transient loss of consciousness
(TLOC) Complete and, typically, rapid recovery
Global cerebral hypoperfusion as the final common pathway regardless
of etiology
• Otherwise, the episode should be referred to as “TLOC” so as to include
nonsyncopal etiologies in the differential diagnosis (Table 6-1).
Epidemio l o gy
• The lifetime incidence of syncope is 30% to 50%.1-3
• It accounts for 3% to 5% of emergency room visits and 1% to 6% of
hospital admissions. Many more cases of syncope are not reported.4
• Large population data showed a rate of 6.2 per 1,000 person-years, with
an
increasing incidence in the elderly. 5 For institutionalized patients over the age
of
70, the incidence is as high as 23% over 10 years.6
Etio l o gy
• Syncope first must be differentiated from nonsyncopal events involving real
or apparent TLOC, such as seizures and falls (Table 6-1).
• Further subdivision of true syncope is based on specific
pathophysiologic etiologies that include the following four general categories
(Table 6-2) in descending order of frequency:
Neurally mediated (reflex) syncope
Orthostatic syncope
Primary cardiac arrhythmias
Structural cardiac or cardiopulmonary disease
DIA GNO SIS
Cl in ic al Pr esen tatio n
• Initial evaluation of syncope utilizes the history, physical examination, and
electrocardiogram (ECG) to classify presumed causes and identify patients
who are at high risk for death. There are three key questions that need to be
answered with the initial evaluation:
86
Is loss of consciousness attributable to syncope or
not? Is heart disease present or not?
Are there important clinical features in the history that suggest the diagnosis?
• In addition, consideration of inpatient versus outpatient evaluation should
depend on comorbidities and initial findings. In general, patients with the
following should be admitted to avoid delay and adverse outcomes:
Elderly (age > 65 years)
Known structural heart
disease
Symptoms suggestive of primary cardiac syncope
Abnormal ECG
Severe orthostatic hypotension
Focal neurological deficits
87
87
Family history of sudden death
Exertional syncope
Syncope causing severe injury
Syncope while driving
Histo ry
• Often, the diagnosis of syncope is evident from the history.
• Aspects of the history that need to be explored in order to aid diagnosis
and further categorize the event include a prodrome before the attack,
eyewitness accounts during the event, the patient’s recollection immediately
after the attack, circumstances that may have played a causative role in the
event, and general questions about the patient’s medical history.
• A helpful mnemonic is, “I passed out on the BEACH” (Table 6-3).
• For patients with recognizable reflex or orthostatic syncope that
occurs infrequently or as an isolated episode, no further workup is
necessary. These patients generally have a good prognosis and can be managed
as outpatients with treatments listed below.
• In patients with a suspected cardiac etiology, an inpatient cardiac
evaluation is warranted.
Ph ysical Examin atio n
• The examination should include assessment of orthostatic vital signs and
careful neurologic, pulmonary, and cardiovascular assessment.
Proper orthostatic vital signs
include
Blood pressure (BP) checked (both arms) after the patient lies supine for
at least 5 minutes
BP measured 3 minutes after standing
Orthostasis = 20-mmHg decrease in systolic BP and/or 10-mmHg decrease
in diastolic BP and/or 10-bpm increase in heart rate (HR)
Cardiovascular findings that may point to cardiogenic syncope
include
Arrhythmias (tachyarrhythmias, bradyarrhythmias, and irregularity)
Murmurs (especially aortic stenosis or hypertrophic
obstructive cardiomyopathy)
Evidence for heart failure (S3, S4, edema, and elevated JVD)
Neurologic findings are often absent, but might include evidence of
autonomic neuropathy (e.g., inappropriate sweating, lack of HR variability,
extreme orthostatic BP changes).
A firm massage at the carotid artery bifurcation for 5 to 10 seconds
may reproduce symptoms, particularly in the elderly.
This maneuver can be performed safely at the bedside with the patient lying
recumbent on telemetry monitoring and appropriate bradycardia treatments
available.
The test is considered positive if it results in a ventricular pause of
>3 seconds.
Neurologic complications are rare (<0.5%), but the procedure should
be avoided in patients with known carotid disease, carotid bruits, or a
recent transient ischemic attack (TIA)/cerebrovascular accident.
Diagn o stic Testin g
• Given the broad differential, the syncope evaluation is notorious for
triggering extensive, multimodality diagnostic testing.
• The 2006 American Heart Association (AHA)/American College of
Cardiology
(ACC) algorithm for cardiac evaluation of syncope is outlined in Figure 6-1.7
El ectro cardio graph y
Specific abnormalities to look for on ECG include
• Evidence of sinus node dysfunction
• Evidence of atrioventricular conduction abnormalities
• Tachyarrhythmias (supraventricular tachycardia [SVT], ventricular
tachycardia
[VT], atrial fibrillation [AF])
• Evidence of ventricular preexcitation (delta waves)
• Evidence of underlying structural heart disease
includes Q waves suggestive of prior myocardial
infection Wide QRS (>120 milliseconds)
Left ventricular hypertrophy pattern suggestive of hypertrophic
cardiomyopathy
(HCM)
Anterior precordial T-wave inversions and/or epsilon waves suggestive
of arrhythmogenic right ventricular dysplasia (ARVD)
• Evidence of
channelopathy: Long or
short QT.
Right bundle branch block with down-sloping ST elevation and T-wave
inversion in V1–V3 (Brugada pattern).
Imagin g
•
The expanded cardiac evaluation includes an echocardiogram, exercise
testing, and an ischemic evaluation.
In appropriate patients, an exercise stress echo would be sufficient to
complete
all three aspects of testing (baseline imaging followed by exercise protocol
and stress imaging).
The echocardiogram alone may be diagnostic in cases of valvular heart
disease, cardiomyopathy, or congenital heart disease.
Exercise testing is preferable to pharmacologic stress and should be
symptom- limited.
Noninvasive
testing
for
ischemia
should
be
followed
by
cardiac catheterization if there is an evidence of ischemia or previously
unrecognized infarction.
• Cardiac magnetic resonance imaging or computed tomography may be helpful
in
the evaluation of structural heart disease, including HCM, ARVD, or
coronary anomalies.
• If an arrhythmic cause is suspected, but not evident on the initial workup or
on expanded cardiac evaluation, ambulatory cardiac rhythm monitoring
can be achieved via one of the following modalities8:
Holter monitor (24 to 48 hours of continuous
recording)
Event recorder (1 month of patient-activated or patient-triggered recordings to
temporally correlate with symptoms)
90
90
Mobile Continuous Outpatient Telemetry (MCOT) for up to one month of
continuous monitoring
Implantable loop recorder (years of continuous
recording)
91
91
FIGU RE 6- 1 . Al go rith m fo r th e eval uatio n o f syn co pe. (Mo dified fro m American Heart Asso ciatio n
/American Co l l ege o f
Cardio l o gy Fo un datio n . AHA/ACCF scien tific statemen to n th e eval uatio n o f syn co pe. Circul atio n 2006;113:316.)
The choice of monitoring is dependent on the frequency of symptoms and type
of suspected arrhythmia. Even in a highly selected population, the diagnostic
yield of ambulatory cardiac monitoring is relatively low.
• Tilt table testing has been used traditionally as a diagnostic tool to characterize
a patient’s hemodynamic response to controlled postural change from
supine to upright state to aid in the diagnosis of a reflex-mediated
(neurocardiogenic) syncope.
Physiologically, there is a large volume shift during repositioning, with 500
to
1000 mL of blood moving from the thorax to the distensible venous system
below the diaphragm within the first 10 seconds.
The hydrostatic pressures created by the upright position result in a
similar volume of fluid moving to the interstitial space within 10 minutes.
Autonomic vasoconstriction is the key reflex to counter this orthostatic
stress, and failure of the vasoconstriction mechanism at any point may
result in syncope.
An under-filled right ventricle will trigger a strong vagal response, leading
to bradycardia and hypotension
Results are classified as primarily vasodepressor, cardioinhibitory, or mixed.
Unfortunately, the test has a low sensitivity and reproducibility. It is
our institutional bias that a tilt table test adds very little to a thorough
history, physical examination, and standard cardiac workup of syncope.
• Electrophysiology studies (EPS) can be useful in selected patients.
Indications for EPS include
Abnormal ECG suggesting conduction system cause
Syncope during exertion or while supine or in the presence of structural
heart disease
Syncope with associated palpitations
Family history of sudden death
To define/ablate identified arrhythmias in patients with high-risk occupations
TREA TMENT
• Treatment of syncope can be broadly defined as preventing recurrences
and
reducing the risk of injury or death.
• In general, this is tailored to treat the suspected underlying etiology of the
syncope.
• Various approaches to treating the four etiologies of syncope are shown in
Table
6-4.
Medic atio n s
• The most common pharmacologic options for preventing venous pooling
and aiding intravascular volume expansion include
Midodrine (2.5 to 10 mg by mouth (PO) three times a day)9,10
Peripheral α-agonist causing both arterial and venous constriction
Adverse effects: paresthesias, piloerection, pruritus, and supine
hypertension Avoid in patients with carotid artery disease (CAD),
peripheral arterial disease, and acute renal failure
The only drug shown effective in trials for orthostatic hypotension and
reflex- mediated syncope
Fludrocortisone (start 0.1 mg PO daily, can increase by 0.1 mg weekly
to
maximum of 1.0 mg PO daily)
Synthetic mineralocorticoid causing sodium retention and volume expansion
Adverse effects: hypertension, peripheral edema, and hypokalemia11
An ongoing randomized control trial (POST II) is investigating
effectiveness in reflex syncope12
β-Blockers are often prescribed for syncope, though trials do not support
this
practice.13
O th er No n ph ar mac o l o gic Th er apies
• For reflex syncope, effective treatment may be as simple as avoiding
syncopal precipitants.
• When such precipitants cannot be avoided, coping strategies can be
helpful.
Isometric muscle contractions can improve venous return and abort frank
syncope in patients with a recognizable prodrome.
Lif estyl e/ Risk Mo dif ic atio n
• Driving restrictions should be discussed in patients with unexplained
syncope when appropriate.
• Recommendations currently vary depending on etiology, underlying disease,
type of license held (private versus commercial), and adequacy of treatment.
• If cause of syncope is an active cardiac arrhythmia, patients should be
instructed not to drive until successful treatment has been initiated and the
patient has received permission from the treating physician.
• In general, in patients with a serious episode of syncope that is not clearly due to
a reversible etiology, guidelines recommend driving restriction for 3 to 6
syncope- free months. Also, federal law and variable state law pertinent to
licensure in these individuals exist and should be consulted when applicable.
O UTCO ME/ PRO GNO SIS
• One-third of the patients with syncope will have a recurrent event within 3 years.
• Select subgroups of patients with noncardiac syncope who have an
excellent prognosis. Young, otherwise healthy individuals with a normal ECG
and without identifiable heart disease have essentially no increased risk of death
relative to the population at large.
• Reflex syncope is associated with no increase in mortality risk.
• Syncope from orthostatic hypotension has an excellent prognosis if the
underlying abnormality is easily identified and treated.
• In contrast, syncope with an identifiable cardiac etiology carries a higher risk
of mortality, particularly in patients with advanced heart failure. Mortality
approaches 45% at 1 year for patients with syncope and left ventricular (LV)
ejection fraction <20%.14
REFERENCES
1. Kenny RA, Bhangu J, King-Kallimanis BL. Epidemiology of syncope/collapse in younger and older
Western patient populations. Prog Cardiovasc Dis 2013;55:357-363.
2. Ganzeboom KS, Mairuhu G, Reitsma JB, et al. Lifetime cumulative incidence of syncope in the
general population: a study of 549 Dutch subjects aged 35-60 years. J Cariovasc Electrophysiol
2006;17:1172-1176.
3. Manolis AS, Linzer M, Salem D, Estes NA, 3rd. Syncope: current diagnostic evaluation and
management.
Ann Intern Med 1990;112:850-863.
4. Shen WK, Decker WW, Smars PA, et al. Syncope Evaluation in the Emergency Department Study
(SEEDS):
a multidisciplinary approach to syncope management. Circulation 2004;110: 3636-3645.
5. Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J
Med
2002;347:878-885.
6. Lipsitz LA, Wei JY, Rowe JW. Syncope in an elderly, institutionalised population. prevalence, incidence,
and associated risk. Q J Med 1985;55:45-54.
7. Strickberger SA, Benson DW, Biaggioni I, et al. AHA/ACCF Scientific Statement on the evaluation
of syncope: from the American Heart Association Councils on Clinical Cardiology, Cardiovascular
Nursing, Cardiovascular Disease in the Young, and Stroke, and the Quality of Care and Outcomes
Research Interdisciplinary Working Group; and the American College of Cardiology Foundation: in
collaboration with
the Heart Rhythm Society: endorsed by the American Autonomic Society. Circulation
2006;113:316-327.
8. Subbiah R, Gula LJ, Klein GJ, et al. Syncope: review of monitoring modalities. Curr
Cardiol Rev 2008;4:4148.
9. Low PA, Gilden JL, Freeman R, et al. Efficacy of midodrine vs placebo in neurogenic
orthostatic hypotension.
A randomized, double-blind multicenter study. Midodrine Study Group. JAMA 1997;277:10461051.
10. Wright RA, Kaufmann HC, Perera R, et al. A double-blind, dose-response study of
midodrine in neurogenic orthostatic hypotension. Neurology 1998;51:120-124.
11. Chobanian AV, Volicer L, Tifft CP, et al. Mineralocorticoid-induced hypertension in
patients with orthostatic hypotension. N Engl J Med 1979;301:68-73.
12. Raj SR, Rose S, Ritchie D, et al.; POST II Investigators. The Second Prevention of Syncope
Trial (POST II)
—a randomized clinical trial of fludrocortisone for the prevention of neurally mediated
syncope: rationale and study design. Am Heart J 2006;151:1186.e11-17.
13. Sheldon R, Connolly S, Rose, et al. POST Investigators. Prevention of Syncope Trial
(POST): a randomized, placebo-controlled study of metoprolol in the prevention of
vasovagal syncope. Circulation 2006;113:11641170.
14. Middlekauff HR, Stevenson WG, Stevenson LW, et al. Syncope in advanced heart failure:
high risk of sudden death regardless of origin of syncope. J Am Coll Cardiol 1993;21:110116.
