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SYNCOPE
LEARNING OBJECTIVES:
At the end of this tutorial, you should be able to:
1. Define syncope
2. Form a differential diagnosis for the aetiology of syncope
3. Outline the causes of syncope and their pathogenesis.
4. Take a history from patients with syncope, looking for features which may
assist in narrowing the differential.
5. Examine patients with syncope to elicit features suggestive of underlying
aetiology.
6. Choosing and justifying appropriate investigations of the patient with
syncope.

DEFINITION: Syncope is defined as a transient, self-limited loss of

consciousness with an inability to maintain postural tone that is followed by
spontaneous recovery.

PATHOPHYSIOLOGY: Syncope occurs due to global cerebral hypoperfusion.

Cerebral perfusion is maintained relatively constant by an intricate and complex
feedback system involving cardiac output, systemic vascular resistance, arterial
pressure, intravascular volume status, cerebrovascular resistance with intrinsic
autoregulation, and metabolic regulation. A clinically significant defect in any
one of these or subclinical defects in several of these systems may cause
syncope.
Cardiac output (CO) can be diminished secondary to mechanical outflow
obstruction, pump failure, arrhythmias, or conduction defects. Systemic
vascular resistance (SVR) can drop secondary to autonomic failure or vasovagal
response. Mean arterial pressure (MAP) decreases with all causes of
hypovolemia. Medications can affect CO, SVR, or MAP.

DIFFERENTIAL DIAGNOSIS:

Arrhythmia (1) Bradycardia (slowness of heart beat)

(2) Sick-sinus (variable)
(3) Supraventricular or ventricular tachycardia
(abnormally fast)

Haemodynami (1) Aortic stenosis

c
(2) Pulmonary embolism or hypertension
Neurally (1) Vasovagal reaction (usually related to emotional
mediated stress)
(2) Carotid sinus hypersensitivity

(3) Postural hypotension (usually related to medication or

dehydration) or related to autonomic
neuropathy(diabetes mellitus)
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Non-Cardiac (1) Seizure

Causes (2) Stroke or TIA
(3) Metabolic encephalopathy

(4) Psychiatric conditions

HISTORY:

History and physical examination are the most specific and sensitive ways to
evaluate syncope. The diagnosis is achieved with a thorough history and
physical examination in 50-85% of patients. No single laboratory test has
greater diagnostic efficacy.

A detailed account of the event must be obtained from the patient. The account
must include the circumstances surrounding the episode: the precipitant
factors, the activity the patient was involved with prior to the event, and the
patient's position when it occurred.

(1) Precipitant factors can include fatigue, sleep or food deprivation, warm
ambient environment, alcohol consumption, pain, and strong emotions
such as fear or apprehension.
(2) Activity prior to syncope may give a clue as to the etiology of symptoms.
Syncope may occur at rest; with change of posture; on exertion; after
exertion; or with specific situations such as shaving, coughing, voiding, or
prolonged standing. Syncope occurring within 2 minutes of standing
suggests orthostatic hypotension.
(3) Assess whether the patient was standing, sitting, or lying when the
syncope occurred. Syncope while seated or lying is more likely to be
cardiac.

The following questions should be answered:

(1) Was loss of consciousness complete?

(2) Was loss of consciousness with rapid onset and short duration?
(3) Was recovery spontaneous, complete, and without sequelae?
(4) Was postural tone lost?
(5) If the answers to these questions are positive, the episode has a high
likelihood of being syncope. If one or more answers are negative,
consider other forms of loss of consciousness prior to proceeding with
syncope evaluation.

The clinician should attempt to gather all information with respect to symptoms
preceding the syncope.
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(1) Prior faintness, dizziness, or light-headedness occurs in 70% of patients

experiencing true syncope. Other symptoms, such as vertigo, weakness,
diaphoresis, epigastric discomfort, nausea, blurred or faded vision, pallor,
or paresthaesias, may also occur in the pre-syncopal period.
(2) Symptoms of nausea or diaphoresis prior to the event may suggest
syncope rather than seizure when the episode was not witnessed,
whereas an aura may suggest seizure.
(3) Patients with true syncope do not remember actually falling to the
ground. Presyncope involves the same symptoms and patho-physiology
but terminates prior to loss of consciousness and can occasionally include
loss of postural tone.
(4) The duration of symptoms preceding a syncopal episode has been
reported to be an average of 2.5 minutes in vaso-vagal syncope and an
average of only 3 seconds in arrhythmia-related cardiac syncope.

Clinicians should specifically inquire as to red flag symptoms, such as exertional

onset, chest pain, dyspnea, low back pain, palpitations, severe headache, focal
neurologic deficits, diplopia, ataxia, or dysarthria prior to the syncopal event.

Patients should be asked to estimate the duration of their loss of consciousness.

Syncope is associated with patient estimates ranging from seconds up to 1
minute in most cases. To discriminate from seizures, patients should also be
asked if they remember being confused about their surroundings after the event
or whether they have oral trauma or incontinence.

A detailed account of the event must also be obtained from any available
witnesses. Witnesses can aid the clinician in differentiating among syncope,
altered mental status, and seizure.

(1) Convulsive activity, automatisms, or attempts to elicit focality can

indicate seizure. Witnesses may be able to estimate the duration of
unconsciousness and to assist in ascertaining whether the patient
experienced postevent confusion.
(2) Post-event confusion is the most powerful tool for discriminating between
syncope and seizure. A postictal phase suggests that a seizure has
occurred.

Medications:

A medication history must be obtained in all patients with syncope with special
emphasis placed on cardiac and antihypertensive medications. Drugs commonly
implicated in syncope include the following:

(1) Agents that reduce blood pressure (eg, antihypertensive drugs, diuretics,
nitrates)
(2) Agents that affect cardiac output (eg, beta-blockers, digitalis, anti-
arrhythmics)
(3) Agents that prolong the cardiac output (QT) interval (eg, tricyclic
antidepressants, phenothiazines, quinidine, amiodarone)
(4) Agents that alter sensorium (including alcohol, cocaine, analgesics with
sedative properties)
(5) Agents that alter serum electrolytes (especially diuretics
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Family history
Enquiry must be made into any personal or familial past medical history of
cardiac disease.

EXAMINATION:

A complete physical examination is required for all patients who present with
syncope.

Always analyze the vital signs. Fever may point to a precipitant of

syncope, such as a urinary tract infection (UTI) or pneumonia. Postural
changes in blood pressure (BP) and heart rate may point toward an
orthostatic cause of syncope but are generally unreliable. Tachycardia
may be an indicator of pulmonary embolism, hypovolaemia,
tachyarrhythmia, or acute coronary syndrome. Bradycardia may point
toward a vasodepressor cause of syncope, a cardiac conduction defect, or
acute coronary syndrome.
Bruising on a patients face often indicates true syncope as the natural
reaction is to put ones hands out when falling, if conscious.
A detailed cardiopulmonary examination is essential. Irregular rhythms,
ectopy, brady-arrhythmias, and tachy-arrhythmias should be detected.
Auscultation of heart sounds may reveal murmurs indicating high-grade
valvular defects. Search for objective evidence of CHF, including jugular
venous distension, lung crepitations, hepatomegaly, and pitting-
dependent oedema. Examine the abdomen for the presence of a pulsatile
abdominal mass.
A detailed neurologic examination assists in establishing a baseline as
well as defining new or worsening deficits. Patients with syncope should
have a normal baseline mental status. Confusion, abnormal behaviour,
headache, fatigue, and somnolence must not be attributed to syncope; a
toxic, metabolic, or CNS cause must be considered. The patient should
have a detailed neurologic examination, including evaluation for carotid
bruits, cranial nerve deficits, motor deficits, deep tendon reflex
lateralization, and sensory deficits.
The patient must be examined for signs of trauma. Trauma may be
sustained secondary to syncope with resultant head injury, lacerations,
and extremity fractures. Tongue trauma is thought to be more specific for
seizures.

INVESTIGATIONS:

Bedside tests:

1. Lying and Standing BP: Orthostatic changes marked by a decrease in

systolic BP by 20 mm Hg, a decrease in diastolic BP by 10 mm Hg, or an
increase in heart rate by 20 beats per minute (bpm) with positional
changes or systolic BP less than 90 mm Hg with the presence of
symptoms may indicate postural hypotension.
2. Hallpike Manoeuvre: The Hallpike manouevre may be performed in
patients to assess for benign paroxysmal positional vertigo.

Bloods:
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1. Glucose: A glucose level, checked by rapid fingerstick testing should be

evaluated in any patient with syncope. Hypoglycaemia can produce a
clinical picture identical to syncope, including the prodromal symptoms,
absence of memory for the event, and spontaneous resolution.
2. Cardiac Enzymes: These tests are indicated in patients who give a
history of chest pain with syncope, dyspnea with syncope, or exertional
syncope; those with multiple cardiac risk factors; and those in whom a
cardiac origin is highly suspected.
3. Creatine Kinase: A rise in CK levels may be associated with prolonged
seizure activity or

Radiological:

1. CT Brain: CT brain may be clinically indicated in patients with new

neurologic deficits or in patients with head trauma secondary to syncope
but it has a very low diagnostic yield in syncope.
2. CTPA: CT Pulmonary Angiogram: This test is appropriate for patients in
whom pulmonary embolus is suspected.

Cardiac:

1. ECG: 12 lead ECG- can be diagnostic for acute MI or myocardial

ischemia and can provide objective evidence of preexisting cardiac
disease or dysrhythmia such as Wolff-Parkinson-White syndrome, Brugada
syndrome, atrial flutter, or AV blocks.
2. Echocardiogram: This is the test of choice for evaluating suspected
mechanical cardiac causes of syncope.
3. Holter: Holter monitor/loop event recorder Most patients will have a 24
hour ECG monitor or holter with the aim of picking up any paroxysmal
arrythmias.Loop recorders allow for monitoring over longer time periods,
which increases the yield of detecting an arrhythmia

Miscellaneous

Tilt table test: This test is useful for confirming autonomic dysfunction and
involves using a tilt table to stand a patient at 70 degrees for 30 minutes and
monitoring for postural hypotension/syncopal episodes. Carotid sinus massage
can also be carried out at this time to look for carotid sinus disease.