Syncope

SYNCOPE
BY;
DR. ZAREEN KIRAN
POST GRADUATE TRAINEE
INTERNAL MEDICINE

DEFINITION
Transient loss of consciousness with loss
of postural tone.
Sudden onset
Brief duration
Spontaneous & complete recovery
Without neurological deficit
Without requiring resuscitation

EPIDEMIOLOGY
3% of emergency visits
6% of medical admissions
1% of all hospital visits
Peak age group in young between 10-
30yrs
Incidence increases after 70yrs in elderly
Common in females
Young often have family history in 1st
degree relative

v/s PRESYNCOPE
Prodromal of syncope
Without loss of postural tone
Typical symptoms are;
dizziness, lightheadedness or faintness,
weakness, fatigue, and visual and auditory
disturbances.

v/s SEIZURES
SYNCOPE
 Upright posture
 Pallor present
 Unconscious-seconds
 Recovery-rapid
 Post-ictal confusion,
amnesia, headache-
ABSENT
 Injury-UNCOMMON
 Tongue biting-NEVER
SEIZURE
 Any posture
 Pallor absent
 Unconscious-minutes/hrs
 Recovery-slow
 Post-ictal confusion,
amnesia, headache-
PRESENT
 Injury-COMMON
 Tongue biting-COMMON

PATHOPHYSIOLOGY
Loss of postural tone-failure of baroreflex
response to upright posture
Loss of consciousness-acute global
impairment of cerebral blood flow

CAUSES OF SYNCOPE
The causes of syncope can be divided into
three general categories:
(1) neurally mediated syncope (also called
reflex syncope),
(2) orthostatic hypotension, and
(3) cardiac syncope.

EVALUATION AND APPROACH
The initial evaluation should answer three
key questions:
Is it a syncopal episode or other type of
event?
Has the etiology been determined?
Is there evidence suggestive of a high risk
of cardiovascular events or death?

CLINICAL PRESENTATION
History
Physical examination
ECG

CLINICAL FEATURES
 History:
The prodromal symptoms
Search for structural heart disease
Myoclonic jerks-due to cerebral anoxia
Vertigo, drop attacks, psychiatric evaluation for
somatization and TIA
 Physical examination:
CVS examination-murmurs, tumor plops
Carotid bruit & Peripheral pulses examination
for subclavian steal syndrome
Clues for collagen vascular disease or
vasculitides
Blood pressure measurement-both arms and for
postural drop

Reproduced with permission from: European Heart Rhythm Association (EHRA), Heart Failure
Association (HFA), Heart Rhythm Society (HRS), et al. Guidelines for the diagnosis and
management of syncope (version 2009): the Task Force for the Diagnosis and Management of
Syncope of the European Society of Cardiology (ESC). Eur Heart J 2009; 30:2631. Copyright ©
2009 Oxford University Press.

DIAGNOSTIC EVALUATION
The 2009 ESC guidelines recommended
the following testing strategy:
Carotid sinus massage in patients >40 years old
Echocardiogram when there is previous known
heart disease or data suggestive of structural
heart disease
Immediate ECG monitoring when there is a
suspicion of arrhythmic syncope
Orthostatic challenge
Other less specific tests such as neurological
evaluation or blood tests-non-syncopal transient
loss of consciousness.

ORTHOSTATIC CHALLENGE
TESTS
 Active standing — Orthostatic blood pressure
measurement is performed with the patient standing
after at least 5 minutes of lying supine. Blood pressure
should be measured each minute (or more often) in the
standing position for three minutes or more (or as long
as the patient tolerates)
 Tilt testing — Tilt testing is commonly performed for
the evaluation of syncope, although the test has limited
specificity, sensitivity, and reproducibility

UPRIGHT TILT-TABLE TESTING
 INDICATIONS:
Recurrent episodes of syncope in the absence of
organic heart disease, or in the presence of
organic heart disease after cardiac causes of
syncope have been excluded.
Unexplained single syncopal episode in high risk
settings (eg, occurrence or potential risk for
physical injury or occupational hazard).
When deemed of clinical value to demonstrate
susceptibility to reflex syncope to the patient.

PROCEDURE:
Electrophysiology laboratory using a special
tilt table
Isoproterenol is infused & nitroglycerin is
given if the initial tilt test is negative
Hydraulic lift or swinging bed capable of
smoothly and rapidly moving the patient
passively from a supine position to a head-
up position between 60º to 90º

Interpretation
 Classic orthostatic hypotension (OH) is defined as a
decrease in systolic blood pressure (BP) of ≥20 mmHg and
in diastolic BP ≥10 mmHg within 3 min of standing. This
syndrome is diagnosed by active standing or tilt testing.
 Initial OH is defined by a BP decrease immediately on
standing of >40 mmHg with BP spontaneously and rapidly
returning to normal, so the period of hypotension and
symptoms is <30 s. This is diagnosed by active standing.
 Reflex syncope (vasovagal syncope) triggered by standing is
characterized by an initial normal adaption reflex followed
by rapid fall in venous return and vasovagal reaction (reflex
bradycardia and vasodilatation). This is diagnosed by tilt
table.

 Delayed (progressive) OH is defined by a slow
progressive decrease in systolic BP on standing with no
bradycardic reflex (in contrast to reflex syncope). This is
diagnosed by tilt table.
 Delayed (progressive) OH plus reflex syncope occurs
when a vasovagal reaction (reflex bradycardia and
vasodilation) follows delayed OH. This is diagnosed by
tilt table.
 Postural orthostatic tachycardia syndrome (POTS)
presents with severe orthostatic intolerance (not
syncope) with marked increase in heart rate (by >30
beats per minute or to >120 beats per minute) and
instability of BP. This is diagnosed by tilt table. This
syndrome is discussed in detail separately.

ECHOCARDIOGAPHY
 Echocardiography is recommended in patients with
syncope when structural cardiac disease is suspected.
 Assessment of cardiac substrate may also help stratify
risk.
 Echocardiography can diagnose underlying structural
heart disease such as left ventricular dysfunction,
hypertrophic cardiomyopathy, or significant aortic
stenosis.

 It may also suggest pulmonary embolism if pulmonary
hypertension or right ventricular enlargement is present.
 However, the finding of structural heart disease
does not generally establish the etiology for syncope
and usually other tests are indicated to determine the
cause.
 Only a finding of severe aortic stenosis, obstructive
tumor or thrombus (eg, atrial myxoma), cardiac
tamponade, aortic dissection, or congenital anomaly of
the coronary artery is considered diagnostic as a cause
for syncope.

ECG MONITORING
In-hospital monitoring
Continuous 24-48 hr/HOLTER monitoring
External event recorder
Implantable loop recorder

 Helpful in excluding arrhythmia as the etiology of syncope if
the patient has symptoms while monitored and no
arrhythmia is recorded.
 Diagnostic when a correlation between syncope and an
arrhythmia (brady or tachyarrhythmia) is detected.
 Excludes an arrhythmic cause when there is a correlation
between syncope and lack of rhythm variation.
 In the absence of such correlations, ECG monitoring is
considered diagnostic when there are
 ventricular pauses longer than 3 seconds or
 periods of Mobitz II or third degree atrioventricular block, or
 rapid prolonged paroxysmal supraventricular or ventricular
tachycardia.

ELECTROPHYSIOLOGICAL STUDY
 INDICATIONS:
In patients with ischemic heart disease, EPS is
recommended when initial evaluation suggests
an arrhythmic cause of syncope, unless there is
already an established indication for an
implantable cardioverter-defibrillator (ICD).
In patients with bundle branch block, EPS
should be considered when noninvasive tests
have failed to make the diagnosis.

INTERPRETATION:
 Sinus bradycardia and prolonged corrected sinus
node recovery time (CSNRT) (>525 ms)
 Bundle branch block and either a baseline His-
ventricle (HV) interval of ≥100 msec or second or
third degree His-Purkinje block during incremental
atrial pacing or pharmacologic challenge. An HV
interval between 70 and 100 may be considered
diagnostic.
 Induction of sustained monomorphic ventricular
tachycardia in patients with prior myocardial
infarction
 Induction of rapid supraventricular tachycardia which
reproduces hypotensive or spontaneous symptoms

ADENOSINE TRIPHOSPHATE
TEST
Patients are injected with 20mg bolus ATP
and kept in supine position with
continuous ECG monitoring.
Asystole lasting longer than 6 seconds or
atrioventricular block lasting longer than
10 seconds is considered abnormal.
Investigational

TREATMENT
Non pharmacological therapy
Medical therapy
Device therapy
Surgical therapy

Non pharmacological
Behavior modification with regard to
changing position from supine to standing
Avoidance of precipitating factors
Avoidance of volume depletion
Exercise training
Correction of electrolytes
Regular check on drug-drug interactions

Medical therapy
Beta blockers, SSRI, disopyramide &
scopolamine have been tried for neurally
mediated(vasovagal) syncope, but with no
evidence from randomized control trials.
Fludrocortisone, midodrine, ephedrine,
desmopressin and methylphenidate for
orthostatic hypotension.
Antiarrhythmic drugs for cardiogenic
syncope.

Surgical therapy
Surgical removal of carotid sinus tumors
Surgical septal myectomy for HOCM
Percutaneous septal ablation with alcohol
for HOCM
CABG or PCI for arrhythmias due to
polymorphic VT

Device therapy
Pacemaker implantation for carotid sinus
syncope and AV blocks
Implantable cardioverter defibrillator for
tachyarrhythmias in patients with
coronary artery disease and left
ventricular dysfunction.

Syncope

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