Vasovagal Syncope Flashcards

1
Q

Define syncope.

A

A relatively sudden, temporary, and self-terminating loss of consciousness, associated with the inability to maintain postural tone, with rapid and spontaneous recovery.

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2
Q

What are the three categories of syncope?

A
  • Neurally mediated reflex syncope
  • Orthostatic
  • Cardiovascular
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3
Q

Define vasovagal syncope.

A

A “common faint” - most common cause of syncope

A type of neurally-mediated, reflex syncope whereby symptomatic hypotension causing syncope occurs due to neural reflex vasodilation and/or bradycardia.

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4
Q

What are the warning signs and symptoms for vasovagal syncope?

A

Warning symptoms:

  • feeling hot/cold,
  • sweaty,
  • tachycardic,
  • short of air,
  • loss of hearing,
  • nausea,
  • change in breathing pattern.

Warning signs:

  • marked pallor,
  • clammy skin,
  • confusion.
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5
Q

What is the pathophysiology of syncope?

A

Sudden cessation of blood flow to the brain (6-10seconds is sufficient) which causes loss of consciousness

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6
Q

What mechanisms of autoregulation are available to maintain cerebral blood flow?

A

MABP between 60-160mmHg autoregulation can maintain sufficient blood flow to the brain. Below this range arterioles and arteries have to constrict. Above this you may get brain swelling.

In healthy young people, cerebral blood flow represents 12% to 15% of resting cardiac output. A sudden cessation of cerebral blood flow for only 6 to 10 seconds –> syncope A sustained decrease in SBP to <60 mmHg –> syncope.

There is (1) neural and (2) chemical control of cerebral blood flow.

Neural:

  • Sympathetic innervation of the main cerebral arteries
  • Parasympathetic (facial nerve) stimulation
  • Central cortical neurons – neurons within the brain itself can release neurotransmitters such as catecholamines that cause vasoconstriction (e.g A, NA)
  • Dopaminergic neurons – local effect to active areas. Innervate pericytes around capillaries and SM around arterioles to contract.

Chemical:

  • pH - lower–> vasodilation
  • CO2 (indirectly)
  • NO - through GTP and cGMP
  • K
  • Adenosine
  • Anoxia
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7
Q

What are the risk factors for vasovagal syncope?

A
  • Prior syncope
  • History of arrhythmias, MI, HF, or cardiomyopathy
  • Severe aortic stenosis
  • Prolonged standing
  • Emotional stress (esp in warm/crowded environment)
  • Hypovolaemia
  • Episode of nausea/vomiting
  • Episode of severe pain
  • Excessively warm closed-in environments e.g. most common places are churches, restaurants, long queues.
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8
Q

What are the clinical features of vasovagal syncope?

A
  • Hx of fainting, provocative factor
  • Pallor - characteristic of vasovagal faints; its absence should therefore make one question the diagnosis
  • Diaphoresis
  • Bradycardia
  • Absence of FHx of sudden death
  • Nausea
  • Lightheadedness
  • Feeling sweaty/clammy
  • Short of air
  • Reduced vision/hearing
  • Palpitations
  • Fatigue after episode but recovery is rapid (unlike seizure)
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9
Q

What are the characteristics of jerky movements in syncope?

A
  • Occur later in the faint, as cerebral oxygen deprivation reaches its most severe state.
  • Affects only some faints
  • Brief in duration
  • Erratic
  • Should not be confused with tonic-clonic seizures
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10
Q

What test can you do to distinguish vasovagal faint from other types of syncope?

A

HUT (head up tilt table testing) supports a diagnosis of VS

Has a specificity of 90%

Does not need to be done if the history is typical for VS but can be used to teach the patient about warning symptoms to prevent future events.

  • Should be done >2hrs fasting and with no medication.
  • ECG and blood pressure monitoring
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11
Q

What investigations should be done in suspected vasovagal syncope?

A

All patients:

  • ECG - or Holter monitor - rules out AV block, bradycardia, asystole, long QT, bundle branch block. Also history features that suggest structural heart disease.
  • Lying and standing blood pressure - after 3mins upright
  • Bloods - Hb, trop, BM, U&Es, creatinine, cortisol (in adrenal insufficiency)
  • Pregnancy test (serum beta-human chorionic gonadotropin)

Other:

  • Valsalva maneouvre - should be normal; may indicate autonomic failure which can cause syncope by orthostatic hypotension
  • Carotid sinus massage - may recreate symptoms
  • Echo - rules out HOCM, AS, poor ventricular function
  • Tilt-table test - body is supported at 60-70 degrees for 20-45mins, isoprenaline may be given too
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12
Q

What is significant postural hypotension?

A
  1. A drop in systolic BP of 20mmHg or more (with or without symptoms).
  2. A drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without symptoms).
  3. A drop in diastolic BP of 10mmHg with symptoms (although clinically less significant than a drop in systolic BP).
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13
Q

What is the first-line management of postural hypotension?

A

Non-pharmacological management to mitigate the symptoms:

  • Withdraw offending medication (either substitution or discontinuation)
  • Rise slowly from supine to sitting to standing position
  • Avoid straining, coughing, and prolonged standing in hot weather
  • Cross legs while standing
  • Squat, stooping forward
  • Raise head of bed 10 to 20 degrees
  • Small meals and coffee in the morning
  • Elastic waist high stocking
  • Increase salt and water intake
  • Exercise, eg, swimming, recumbent biking, and rowing
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14
Q

What is the medical management of postural hypotension?

A

Fludrocortisone - acts by expanding blood volume and reducing salt loss

Midodrine - only recommended for autonomic dysfunction causing orthostatic hypotension and when other treatments are inadequate

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15
Q

Why might BPH predispose to syncope?

A

Patient may be taking alpha-blockers which predispose to VVS or postural hypotension

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16
Q

What is glossopharyngeal neuralgia?

A
  • An unusual pain syndrome associated with syncope
  • Episodic sensations of usually left-sided pharyngeal pain

NB: trigeminal neuralgia does not cause syncope

17
Q

What is the management of vasovagal syncope?

A
  • Patient education about prevention
  • Alter medications if increasing risk

Physical techniques

  • Physical counter pressure manoeuvres -abort imminent orthostatic faints e.g. squatting, arm tensing, leg crossing
  • Standing training - progressively longer durations over 3months

Medical therapy

  • Volume expansion - staying hydrated, increased salt and electrolytes, fludrocortisone.
  • Beta-blockers - diminish adrenergic surge so prevent vasovagal trigger
  • Midodrine, etilefrine, methylphenidate - vaso- and venoconstrictor

Surgical therapy

  • Carotid pacing - prevent severe bradycardias in those with refractory syncope
    *
18
Q

What are the side effects of fludrocortisone?

A

Hypertension and hypokalaemia

19
Q

What are the complications of vasovagal syncope?

A

Injuries and fractures

Extradural or cerebral haemorrhage secondary to trauma

20
Q

What is the prognosis with vasovagal syncope?

A

Recurrence is common in about a third

Usually good prognosis compared to cardiac causes of syncope