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Ovid: Manual of Intensive Care Medicine

Editors: Irwin, Richard S.; Rippe, James M.


Title: Manual of Intensive Care Medicine, 4th Edition
Copyright 2006 Lippincott Williams & Wilkins
> Table of Contents > II - Cardiovascular Problems and Coronary Care > 32 - Syncope

32
Syncope
William H. Maisel
Author
Patrick O'Gara
Editor

I. GENERAL PRINCIPLES

Definition: Sudden/transient loss of consciousness with loss of postural tone.

Accounts for 3% of emergency room visits and 1% to 6% of all hospital admissions.

Cost of diagnosis and treatment approaches $750 million dollars per year.

II. PATHOPHYSIOLOGY

Caused by hypoxia/hypoperfusion of the cerebral cortices and reticular activating system.

Systolic blood pressure less than 70 mm Hg or interruption of cerebral blood flow for 8 to 10 seconds
usually results in syncope.

Seizures cause loss of consciousness through global interruption of cerebral electrical activity without
necessarily impairing blood flow.

III. DIAGNOSIS

Differential diagnosis

A number of different disease processes can cause syncope (Table 32-1).

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Reflex mediated syncope and orthostatic intolerance are most common, whereas neurological,
cardiovascular, and psychogenic causes occur with decreasing frequency.

Up to 45% of patients will be labeled as having syncope of unknown cause despite a thorough
evaluation.

Etiology of syncope has important prognostic significance

In absence of implantable defibrillator, syncope of cardiac etiology has 1-year mortality of 20% to
30% compared with 0% to 12% for patients with noncardiovascular causes of syncope and 6%
for those with syncope of unknown etiology.

Younger patients more frequently have syncope due to noncardiovascular cause or syncope of
unknown origin and overall have a more favorable prognosis.

Older patients more often have a cardiac etiology or syncope due to polypharmacy.

Initial diagnostic evaluation

Algorithm for the approach to the patient with syncope (Fig. 32-1).

Goal is to differentiate between benign and potentially life-threatening causes.

Presence of cardiovascular disease identifies patients at increased risk of sudden death.

History and physical examination alone allow diagnosis of syncope cause in 45% of patients and
suggest a diagnosis in another 40%.

History

Obtain patient's and eyewitnesses' reports of event.

Search for situational or provocative factors, postural or exertional symptoms, and symptoms of
cardiac or neurologic origin.

Take a careful medication history.

Past medical history should focus on prior syncopal events, as well as prior cardiac, neurologic,
and psychiatric history.

Family history for familial cardiomyopathy, sudden cardiac death, or syncope should also be
sought.

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TABLE 32-1 Differential Diagnosis of Syncope


Cardiovascular
Arrhythmia

Low cardiac output

Bradyarrhythmia
Sinus node disease

Obstruction to flow
Aortic stenosis

AV node disease

Mitral stenosis

Drug induced
Pacemaker malfunction

Tricuspid stenosis
Hypertrophic cardiomyopathy
Atrial myxoma

Tachyarrhythmia

Pulmonary stenosis

Ventricular arrhythmias
Supraventricular arrhythmias

Pulmonary embolism
Pulmonary hypertension
Cardiac tamponade

Aortic dissection
Pump failure (cardiomyopathy, MI)
Disorders of autonomic control
Autonomic insufficiency
Diabetes mellitus
Parkinson's disease
Primary
Reflex mediated
Neurocardiogenic (vasovagal/vasodepressor)
Carotid sinus hypersensitivity
Situational (cough, defecation, micturition, swallow)
Neuralgia (trigeminal, glossopharyngeal)
Neurologic
Psychiatric
Cerebrovascular disease (CVA, TIA)

Anxiety disorder/panic disorder

Seizure
Hyperventilation

Major depression
Somatization

Migraine

Mnchhausen's

Narcolepsy

Substance abuse

Subclavian steal
Orthostatic hypotension

Metabolic

Volume depletion

Hypoadrenalism

Medication related

Hypoglycemia
Hypothyroidism
Hypoxia

AV, atrioventricular; CVA, cerebrovascular accident; MI, myocardial infarction; TIA,


transient ischemic attack.
P.175

Tongue biting, aching muscles, or disorientation following a syncopal episode suggests a seizure,
whereas sweating, nausea, vertigo, incontinence, injury, headache, family history of epilepsy, and
history of prior concussion are not predictive of seizures.

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Figure 32-1. Algorithm for the approach to the patient with syncope.

P.176

Physical examination

Should focus on identifying potential clues as to the etiology of the syncopal episode.

Orthostatic hypotension as etiology of syncope should be diagnosed only when the history and
examination are consistent and other potential etiologies of syncope have been excluded.

Murmurs, bruits, signs of heart failure, and so forth might suggest cardiovascular etiology.

Neurologic abnormalities such as diplopia, headache, or other focal signs may suggest a
neurologic etiology.

12-Lead electrocardiogram (ECG)

Half the patients who present with syncope have significant baseline ECG abnormalities.

The ECG alone is diagnostic of the cause of syncope in less than 10% of cases.

An abnormal ECG suggests the presence of underlying heart disease and warrants further
evaluation.

The ECG is the only way to diagnose some genetic disorders, including long QT syndrome and

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Brugada syndrome.

Laboratory tests

Routine laboratory evaluation not recommended.

Blood chemistries and hematologic assessments are appropriate as guided by the history and
physical examination.

Further cardiac evaluation (Table 32-2)

Telemetry/24-hour Holter monitoring

Diagnostic in up to 20% of selected patients (symptoms during monitoring either with or


without arrhythmia).

The majority of patients have no symptoms and no arrhythmia during monitoring.

Patient-activated loop recorders, event monitors, and implantable recorders can be used for
patients with infrequent but recurrent episodes.
TABLE 32-2 Indications for Cardiac Tests in Patients with Syncope
Test

Indication

Electrocardiogram
Echocardiogram

All patients at initial presentation


Patients with known or suspected cardiac disease
(including patients with chest pain, heart murmur,
abnormal electrocardiogram, etc.)

Exercise tolerance test

Patients with chest pain, ischemic changes on


electrocardiogram, or exercise-induced or
postexertional syncope (who do not undergo cardiac
catheterization)

Tilt table test

Patients with recurrent syncope or patients with a


single episode of syncope accompanied by physical
injury, motor vehicle accident, or high-risk setting
(pilot, surgeon, window washer, etc.) thought to be
vasovagal. Indicated in patients with unexplained
syncope after other appropriate workup.

Holter or inpatient ECG telemetry

Patients with symptoms suggestive of arrhythmic


syncope (brief loss of consciousness, no prodrome,
presence of palpitations), unexplained cause of
syncope, underlying heart disease, or an abnormal
electrocardiogram

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Electrophysiologic studies

Patients with known or suspected structural heart


disease and unexplained syncope or patients with no
organic heart disease but recurrent syncope and a
negative tilt table test
P.177

Echocardiography

Part of the initial evaluation for patients with known or suspected cardiac disease.

Unselected patients have unanticipated findings 5% to 10% of the time.

Exercise testing

Part of the initial evaluation of patients with suspected ischemia or exercise-induced


arrhythmias

Rarely reveals the precise cause of syncope (less than 1% have an arrhythmia during
exercise testing).

Electrophysiology (EP) studies

Well established for detecting ventricular and supraventricular arrhythmias but less
sensitive for detecting bradyarrhythmias.

Diagnostic yield is approximately 30% to 50% in patients with syncope.

Low yield in patients without structural heart disease.

Patients with normal hearts and normal ECGs rarely require electrophysiology testing.

A positive EP study predicts an increased 3-year sudden death and total mortality rate
compared to patients with negative EP studies.

EP studies are insensitive for the detection of arrhythmias in nonischemic cardiomyopathy.

Signal average ECG (SAECG) and T wave Alternans

Noninvasive test used to identify higher and lower risk patients.

May be considered as an adjunct to other tests in the evaluation for arrhythmia, but it is not
routinely indicated

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Evaluation for disorders of autonomic control/reflex-mediated syncope

A number of syncope syndromes are related to abnormal control of autonomic function (see Table
32-1).
P.178

More than 50% of patients with syncope of undetermined etiology may have neurally mediated
syncope.

Tilt table test

May be used to diagnose neurocardiogenic (also known as vasodepressor or vasovagal)


syncope.

Among patients with syncope of unknown origin, 25% to 50% will have positive tilt table
tests with passive tilt alone, and up to two thirds will have positive tests with the use of
isoproterenol.

False-positive (10% to 30%) and false-negative (30% to 35%) test results are common.

Carotid sinus massage

Performed by firm massage of the carotid artery for 5 to 10 seconds in an attempt to elicit a
baroreflex-mediated vagal response that can cause bradycardia and/or hypotension.

A positive test is: 3 or more seconds of asystole, a 50 mm Hg or greater systolic blood


pressure decrease, or a 40 beats per minute or greater decrease in heart rate.

Should not be performed in patients with a carotid bruit, recent myocardial infarction,
recent stroke, or history of VT.

Neurologic evaluation

Patients with focal neurologic signs or symptoms should undergo further evaluation.

Additional neurologic testing is rarely indicated in the absence of specific clinical abnormalities or
suspicion.

Electroencephalography (EEG)

Yields diagnosis of seizure disorder in less than 2% of unselected patients with syncope
referred for EEG.
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Not recommended as part of the routine evaluation of patients with syncope but should be
considered when seizure is strongly suspected.

Head computed tomography (CT)

Yields a positive finding in less than 5% of patients with syncope.

Unsuspected central nervous system abnormalities are found in less than 1% of patients
without neurologic abnormality on history or physical examination.

Should be reserved for patients with neurologic abnormality and those who have suffered
head trauma.

Psychiatric evaluation

Up to 25% of patients with syncope of unknown etiology have a Diagnostic and Statistical Manual
of Mental Disorders, fourth edition (DSM-IV) psychiatric diagnosis of panic disorder, generalized
anxiety disorder, or major depression.

Screening for psychiatric disorders is recommended for patients with recurrent syncope of unclear
etiology.

IV. TREATMENT

Hospital admission is suggested for patients with syncope who have:

A history or suspicion of coronary artery disease, chronic heart failure (CHF), or ventricular
arrhythmia

Physical signs of significant valve disease, CHF, stroke, or focal neurological disorder

ECG findings of ischemia, arrhythmia, increased QT interval, or bundle branch block

Syncope with injury, rapid heart action, chest pain, or exertion

Frequent episodes

Moderate to severe orthostatic hypotension

Age greater than 70


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Intensive care unit (ICU) admission should be strongly considered in syncope patients with sustained
ventricular tachycardia (VT), symptomatic nonsustained VT, second- or third-degree heart block, pauses
greater than 3 seconds, symptomatic
P.179
bradycardia, severe aortic stenosis, severe CHF, evidence of acute ischemia, or ongoing hemodynamic
instability.

Specific treatment

Arrhythmia. Guidelines for implantation of permanent pacemakers and implantable cardioverterdefibrillators for patients with syncope are summarized in Table 32-3.

Neurally mediated syndromes

Primary treatment is hydration and salt repletion.

b-Adrenergic blockers, selective serotonin-reuptake inhibitors (e.g., fluoxetine), and aadrenergic agonists (midodrine) have demonstrated efficacy in randomized trials.

Other agents, including volume expanders (e.g., fludrocortisone) and disopyramide, appear
useful in some patients.

Patients with recurrent, medically refractory vasovagal syncope associated with marked
bradycardia may benefit from implantation of a permanent pacemaker.

Can consider pacemaker implantation in patients with severe bradycardic response to


carotid sinus massage after other potential causes of syncope are excluded.
TABLE 32-3 Current ACC/AHA Guidelines for Implantation of Permanent Pacemakers
and Implantable Cardioverter-Defibrillators in Patients with Syncope
Device

Pacemaker

Indications for implantation

Symptomatic sinus pauses or sinus bradycardia (I)


Bradycardia and second- or third-degree AV block (I)
Recurrent syncope caused by carotid sinus stimulation; minimal carotid
sinus pressure induces ventricular asystole of >3 seconds duration in the
absence of any medication that depresses sinus node or AV conduction (I)
Major abnormalities of sinus node function or AV conduction discovered or
provoked at electrophysiology study (IIa)
Chronic bifascicular or trifascicular block and syncope not proved to be due
to AV block when other likely causes have been excluded, specifically VT
(IIa)
Recurrent syncope without clear provocative events and with a
hypersensitive cardioinhibitory response (IIa)
Neurally mediated syncope with significant bradycardia reproduced by a
head-up tilt with or without isoproterenol or other provocative maneuvers

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(IIb)

ICD

Clinically relevant, hemodynamically significant sustained VT or VF induced


at electrophysiology study when drug therapy is ineffective, not tolerated,
or not preferred (I)

Ventricular dysfunction and inducible ventricular arrhythmias at


electrophysiologic study when other causes of syncope have been
excluded (IIb)

Indication class in parentheses


Class I: Evidence and/or general agreement that treatment is beneficial
Class IIa: Conflicting evidence and/or divergence of opinion but weight of evidence/
opinion is in favor of treatment
Class IIb: Conflicting evidence and/or divergence of opinion with treatment efficacy less
well established
ACC, American College of Cardiology; AHA, American Heart Association; AV,
atrioventricular; ICD, implantable cardioverter-defibrillator; VT, ventricular tachycardia;
VF, ventricular fibrillation
P.180

Psychiatric causes. Treatment of the underlying psychiatric disorder abolishes recurrent episodes
in most patients.

Special considerations

Patients suspected of having arrhythmic syncope should not drive, pending diagnosis and
treatment.

Many states require a 3- to 12-month driving restriction following a syncopal episode.

State laws vary with respect to the patient's and physician's responsibility to report individuals
with syncope to their respective department of motor vehicles. Physicians should become familiar
with their local requirements.

Selected Readings
Benditt DG, Ferguson DW, Grubb BP, et al. Tilt table testing for assessing syncope. JACC 1996;28:263275.
An excellent review of tilt table testing.

Calkins H. Pharmacologic approaches to therapy for vasovagal syncope. Am J Cardiol 1999;84:20Q25Q.


Excellent review of treatment options for vasovagal syncope.

Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA guidelines for implantation of cardiac pacemakers and
antiarrhythmia devices: Executive summary. Circulation 1998; 97:13251335. Guidelines for which syncope
patients should be treated with device therapy.

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Grubb BP. Pathophysiology and differential diagnosis of neurocardiogenic syncope. Am J Cardiol


1999;84:3Q9Q. Comprehensive overview of neurocardiogenic syncope.

Kapoor WN. Evaluation and management of the patient with syncope. JAMA 1992; 268:25532560. Classic
article on syncope.

Kapoor WN. Syncope. N Engl J Med 2000;343:18561862. Classic article on syncope.

Linzer M, Yang EH, Estes III NAM, et al. Diagnosing syncope part 2: unexplained syncope. Ann Intern Med
1997;127:7686. A review of how to approach the challenge of the patient with unexplained syncope.

Linzer M, Yang EH, Estes III NAM, et al. Diagnosing syncope part 1: value of history, physical examination,
and electrocardiography. Ann Intern Med 1997;126:989996. An excellent review of the diagnostic
evaluation of patients with syncope.

Maisel WH, Stevenson WG. Syncopegetting to the heart of the matter. N Engl J Med 2002;347:931933.
A brief review of the approach to the syncope patient.

Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med
2002;347:878885. A comprehensive study on the incidence and prognosis of syncope in the modern era.

Zipes DP, DiMarco JP, Gillette PC, et al. ACC/AHA guidelines for clinical intracardiac electrophysiological and
catheter ablation procedures. Circulation 1995;92:675691. Guidelines to help assist decision making
regarding which syncope patients require invasive evaluation.

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