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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
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Syncope
Prashant Vaishnava* and Marc Miller*
Key Pearls
• The most common cause of syncope is neurocardiogenic (i.e. vasovagal),
and the primary purpose of the evaluation of the patient presenting with
syncope is to exclude the presence of underlying structural heart disease.
• A meticulous history and directed physical examination are paramount in identifying the cause of syncope.
• The presence of prodrome or postepisode fatigue are the hallmarks of
neurocardiogenic syncope.
• The diagnosis of an arrhythmic cause of syncope hinges upon the
ECG documentation of a rhythm disturbance at the time of symptoms,
and the frequency of symptoms dictates the type and duration of
ambulatory monitoring.
• The clinical utility and diagnostic yield of tilt table testing and electrophysiologic testing is low, particularly in patients with no underlying structural heart disease.
Introduction
Failure of the systemic circulation to generate adequate cerebral hypoperfusion may result in syncope, a transient and brief loss of consciousness
associated with a loss of postural tone and followed by spontaneous recovery. While syncope is a common symptom, accounting for up to 6% of
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Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
hospitalizations, an underlying cause is not identified in up to one-third of
patients. Meticulous history and directed physical examination are paramount in the evaluation and should center upon establishing the presence
of arrhythmia or structural heart disease, which have emerged as the most
important predictors of death among patients presenting with syncope.
1–4
In the general population, the most common cause of syncope is vaso-
vagal or neurocardiogenic, a phenomenon associated with hypotension
and/or bradycardia.
5–7
The gold standard for diagnosing an arrhythmic
cause of syncope is electrocardiographic (ECG) demonstration of the
rhythm disturbance at the time of symptoms. The type and duration of
ambulatory ECG monitoring — Holter, event, or implantable loop monitoring — is dictated by the frequency of symptoms. Tilt table testing and
electrophysiologic studies, while limited by variable sensitivity, specificity and diagnostic yield, may be useful aids in the evaluation of syncope for select patients.
Patient History
Meticulous history taking begins with establishing that syncope is actually the presenting complaint by excluding dizziness, presyncope and
vertigo, which do not result in a loss of consciousness or postural tone.
Emphasis should be given to the circumstances immediately preceding
the syncopal episode and may suggest a particular etiology. A sequential
record of the details of the event, including eyewitness descriptions, is
often useful. A loss of consciousness that is precipitated by pain, exercise, micturition, defecation, deglutition, or stress is often neurocardiogenic in origin.
Neurocardiogenic, or vasovagal, syncope is triggered by a reflex
increase in vagal efferent activity and sympathetic withdrawal. Often the
first sign of impending vasovagal syncope, facial pallor, results from
reduced skin blood flow occurring secondary to vasoconstriction mediated by the sympathetic nervous system. This is followed by other premonitory signs and symptoms, which include diaphoresis, restlessness,
and difficulty with concentration.
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P. Vaishnava and M. Miller
A prolonged period of unconsciousness (often exceeding five minutes), observed rhythmic or clonic movements, and disorientation after
the event may indicate seizure as the diagnosis. Tonic-clonic movements
may also be seen in non-neurological causes of syncope. Transient
ischemic attacks rarely result in syncope, though in the presence of
occlusive carotid artery disease, hypotensive transient ischemic attacks
have been reported. Posture-related syncope is often ascribed to orthostatic hypotension. Volume depletion, medications that alter vascular
tone and heart rate, neurodegenerative diseases (e.g. Parkinson’s disease), or secondary autonomic dysfunction (as seen in diabetes mellitus)
may result in orthostatic hypotension. Carotid sinus hypersensitivity is a
consideration, particularly with an aging population, and should be suspected with syncope provoked by head rotation or pressure on the carotid
sinus (as with tumors, shaving, or tight collars).
8
A careful medication
history may reveal the addition of new drugs, particularly antiarrhythmic
or antihypertensive agents, which may provoke proarrhythmia or
orthostasis, respectively.
Physical Examination
Physical examination may also provide important clues that point toward
a particular cause for the syncope. Blood pressure and heart rate in the
supine, sitting, and standing positions, initially and after three minutes
with attention to reproduction of symptoms, may suggest orthostatic
hypotension. Evaluation of the carotid impulse may suggest aortic stenosis if it is parvus or tardus, and the presence of a carotid bruit may signify
obstructive carotid arterial disease. Carotid sinus massage in the supine
and/or upright positions leading to an exaggerated drop in heart rate may
suggest carotid sinus hypersensitivity, but should not be attempted in the
patient with a suspected ipsilateral carotid artery stenosis or recent cerebrovascular accident. Cardiovascular examination may reveal a harsh
crescendo-decrescendo systolic murmur with softening of the second
heart sound that is consistent with aortic stenosis. Alternatively, a systolic
murmur that intensifies with the Valsalva maneuver is associated with
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P. Vaishnava and M. Miller
Table 1. Clinical Features Suggestive of Specific Causes of Syncope
Historical Features
Loss of consciousness precipitated or following Neurocardiogenic
pain, exercise, micturition, defecation,
deglutition, or stress
Facial pallor Neurocardiogenic
Premonitory signs, including diaphoresis, Neurocardiogenic
restlessness, nausea, or difficulty with
concentration
Prolonged period of unconsciousness (often Seizure
exceeding 5 min)
Observed rhythmic or clonic movements Seizure
Antecedent history of volume depletion Orthostatic hypotension
Known history of neurodegenerative disease Orthostatic hypotension/autonomic
insufficiency
Loss of consciousness provoked by head Carotid sinus hypersensitivity
rotation or with massage on the carotid sinus
(as with shaving or tight collars)
Objective Features
Relative hypotension in the standing position, Orthostatic hypotension
when compared to supine and sitting positions
Parvus and/or tardus carotid arterial pulse Aortic stenosis
Carotid bruit Obstructive carotid arterial disease
Exaggerated decrement in heart rate with Carotid sinus hypersensitivity
carotid sinus massage (if not contraindicated)
Systolic murmur with softening of the second Aortic stenosis
heart sound
Focal, localizing, and/or dynamic signs Cerebrovascular accident
hypertrophic cardiomyopathy, from which a dynamic left ventricular
outflow tract obstruction may result in syncope. Neurological assessment
may suggest focal, localizing, or dynamic signs or symptoms that suggest
a cerebrovascular accident; alternatively, neurodegenerative diseases like
Parkinson’s disease may result in autonomic insufficiency and are associated with particularly abnormal cognition and speech, motor strength,
tremor and gait.
Table 1 contains a summary of the clinical features that are suggestive
of specific causes of syncope.
6
Cardiac Syncope: Arrhythmia and Structural Heart Disease
Abnormalities in cardiac rhythm or structural heart disease with obstruction of cardiac output may lead to syncope. In contrast to the prodromal
symptoms that generally characterize vasovagal syncope, suddenness of
onset without premonitory signs may be suggestive of syncope provoked
by arrhythmias. Certain obstructive lesions (e.g. aortic stenosis or hypertrophic cardiomyopathy) may be associated with exertional syncope.
Obstruction of cardiac output and arrhythmias frequently co-exist.
Among the pathologic entities that may lead to obstruction of cardiac
output, aortic stenosis and hypertrophic cardiomyopathy warrant particular consideration, as follows:
1) Aortic stenosis: Angina pectoris, syncope, and heart failure are the
classic symptoms of aortic stenosis. Once these symptoms develop,
survival is limited; the median survival is only three years after syn-
cope develops.
2) Hypertrophic cardiomyopathy (HCM): An important cause of sud-
den cardiac death among younger patients, HCM is a genetically
determined myocardial disease. Syncope is a particularly ominous
occurrence among patients with HCM and may result from supraven-
tricular or ventricular arrhythmias, bradyarrhythmias, outflow tract
obstruction, or an abnormal hemodynamic response to exertion.
Arrhythmic causes of syncope need to be considered. Bradyarrhythmias
may occur as a consequence of either sinus node dysfunction or disorders
of atrioventricular (AV) conduction. Regarding the former, sick sinus
syndrome may manifest as sinus bradycardia or sinoatrial exit block.
Bradycardia-tachycardia syndrome, in which there are features of sinus
node disease and atrial arrhythmia, may frequently lead to syncope at the
termination of the tachyarrythmia when there is overdrive suppression of
the sinoatrial node. There are varying degrees of atrioventricular block,
with different pathophysiologic mechanisms, electrocardiographic manifestations, and clinical consequences. First-degree atrioventricular block,
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Syncope
generally the result of delayed conduction within the AV node, appears as
prolongation of the PR interval > 200 millseconds and carries an excellent
prognosis.
Second-degree AV block of the Wenckebach type (i.e. Mobitz type 1)
carries a similarly good prognosis, owing to an infra-nodal site of disease.
Its electrocardiographic hallmark is progressive prolongation of the P–R
interval prior to a nonconducted P wave (Fig. 1). The electrocardiographic
hallmark of Mobitz type 2 second-degree AV block is a constant
PR interval prior to a nonconducted P wave, and is generally caused by a block in
the His-Purkinje system (Fig. 2). This form of atrioventricular block may
often result in syncope and generally warrants permanent pacing, unless a
reversible cause is apparent. Similarly, third-degree heart block is characterized by failure of all atrial activity to conduct to the ventricles, and it is
manifested by atrioventricular dissociation (Fig. 3).
Just as bradyarrhythmias may reduce cardiac output and lead to cerebral hypoperfusion, ventricular tachycardia may lead to arrhythmic
syncope. This malignant arrhythmia generally occurs in patients with
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P. Vaishnava and M. Miller
Fig. 1. Mobitz Type 1 AV block.
Fig. 2. Mobitz Type 2 second degree AV Block.
underlying structural or ischemic heart disease (Fig. 4). On surface
electrocardiography, the hallmarks of ventricular tachycardia include
atrioventricular dissociation, easily discernible widening of the QRS complex, and concordance of QRS deflection. And while ventricular arrhythmias generally occur among those with diseased hearts, they may also be
provoked by inherited channelopathies, in the absence of structural heart
disease, and lead to syncope and sudden death.
The Long QT-syndrome (LQTS) and Brugada syndrome are two such
channelopathies. LQTS, characterized by a prolongation of the corrected
QT interval, QTc, to greater than 450 milliseconds may lead to syncope,
presumably secondary to an episode of torsades de pointes, a polymorphic
ventricular tachycardia (Fig. 5). Brugada syndrome, a heritable disorder of
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Syncope
Fig. 3. Complete heart block.
Fig. 4. Ventricular tachycardia.
the cardiac sodium channel, may also lead to syncope and is associated
with characteristic electrocardiographic changes of ST elevation in the
anterior precordial leads with an incomplete right bundle branch block.
The distinctive ECG changes may be dynamic and/or provoked by certain
factors (e.g., cocaine). Supraventricular tachyarrhythmias rarely cause syncope, unless there is concomitant cardiovascular disease, such as an
obstruction to cardiac output.
Select Options for Monitoring and Diagnostic Evaluation
• Routine laboratory testing: Blood tests may reveal anemia or
electrolyte derangements. Electrolyte deficits may cause or aggravate
arrhythmias.
• Noninvasive electrocardiographic monitoring: A single resting
ECG infrequently reveals the cause of a particular syncopal episode.
Inpatient telemetry monitoring may reveal culprit arrhythmias more
frequently. Often, noninvasive ambulatory ECG monitoring is neces-
sary. Continuous Holter monitoring (for up to 72 hours) may reveal an
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P. Vaishnava and M. Miller
Fig. 5. Long QT.
arrhythmic cause of syncope in up to 5% of patients. Long-term
monitoring (lasting weeks or months) is often necessary, as rhythm
disturbances may be transient.
• Echocardiography: When the presence or absence of an underly-
ing structural heart disease cannot be determined by history and
physical examination, transthoracic echocardiography may be indi-
cated and offers valuable insight into biventricular and valvular
function.
• Electrophysiologic testing: Such testing may allow for evaluation of
sinus and AV node conduction, along with susceptibility to ventricu-
lar tachyarrhythmias, in patients thought to be at particularly high risk
for recurrence of arrhythmic syncope. Candidates for electrophysio-
logic testing must be thoughtfully selected, as the yield of such
invasive testing is particularly low among patients with no structural
heart disease.
• Tilt table testing: Limited by its sensitivity, head-up tilt table testing
may be a means to diagnose neurocardiogenic syncope in the setting
of unexplained recurrent syncope. Tilt table testing is of limited value
among individuals in whom the diagnosis of neurocardiogenic syn-
cope is already strongly suggested on the basis of history-taking and
physical examination.
• Neurologic testing: Computed tomography or magnetic resonance
imaging of the brain may be indicated when a neurological basis of
syncope is suspected and when focal neurologic findings are present.
An electroencephalogram leads to a diagnosis in less than 2% of cases
of syncope and is of limited utility.
• Implantable device interrogation: Patients with implanted devices
(i.e. permanent pacemakers or cardioverter-defibrillators) presenting
with syncope may benefit from bedside interrogation of their device
when an arrhythmic cause of syncope is suspected. Bedside interro-
gation may also yield valuable information about the device’s battery
life and ability to sense intrinsic activity and capture appropriately.
Manufacturer-specific device programmers are available.
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Syncope