Clinical:Syncope

Introduction

Syncope is strictly any (sudden) loss of consciousness from generalised cerebral ischaemia rather than the popular definition of a temporary loss of consciousness ^[1].

In assessing syncope in those that have recovered consider:

• The history is extremely important and a witness can give important information as the setting and the immediate events before, during and after are crucial to differentiate the many causes.
• Drug and situational history
• Measuring the postural BP ie lying vs standing if the syncope occurred while upright
• Jerks do not necessarily imply epilepsy - anoxic myoclonic seizures may accompany any cause of cerebral ischaemia.
• Vasovagal syncope is probably the most common cause and is often obvious from the history/examination - it generally needs no further assessment.
• Cardiac arrhythmia should be considered where syncope is triggered by exercise or accompanied by chest pain/palpitations

Aetiology

Any condition or pathology that can cause sudden and profound global cerebral ischaemia could be responsible. The underlying mechanisms involve either a fall in the blood pressure below that necessary for cerebral function or hypoxia. In practice circulatory dysfunction is more likely to induce rapidly reversible syncope than hypoxia.

Common Causes

• Vasovagal syncope or neurocardiogenic syncope is the common faint associated with a abnormal, but very common, stress response of the autonomic nervous system. This response causes inappropriate bradycardia or hypotension or both together. Technically it is one of the neurally-mediated reflex syncopes which can have either a reasonably pure cardioinhibitory response, baroreceptor response or mixture of the two.
• Carotid sinus syncope, also known as carotid sinus syndrome is associated with abnormal sensitivity to external pressure over the region of the carotid sinus autonomic sensory organ at the bifurcation of the external and internal carotid arteries in the neck. This is also a reflex syncope.
• Orthostatic hypotension. Consider:
  • Hypotensive effects of drugs:
    • Alcohol
    • Multiple cardiovascular drugs including all used to treat hypertension
    • Dopaminergic drugs
    • Thalidomide
  • Volume depletion
    • Massive hemorrhage
    • Diarrhoea
  • Autonomic failure owing to diabetes, drugs or multiple systems atrophy (MSA)
• Cardiac arrhythmia
  • Asystole of the order of 3 seconds, with complete heart block or sinus bradycardia aggravated by drugs (eg beta blockers) being common
  • Tachycardia with loss of effective ventricular contraction.
    • Ventricular tachyarrhythmias being the most important to consider although they are often over excluded by investigation as they are unlikely in the absence of other history or findings of heart disease, particularly a normal ECG

Rare Important Causes

Always should be considered as underlying condition common and treatable:

• Myocardial infarction
• Pulmonary embolism
• Aortic stenosis
• Tension pneumothorax

Rarer Causes

• Post prandial syncope
• Micturition syncope
• Tussive syncope induced by coughing fits, also called laryngeal syncope.
• Laughter-induced syncope.
• Defaecation syncope
• Structural heart disease
  • Cyanotic heart disease
  • HOCM
  • Pericardial tamponade
  • Atrial myxoma
  • Long QT syndrome
• Impaired circulation
  • Pregnancy
  • Tumour causing pressure on vena cava
  • A-V shunt
  • Arterial steal syndrome
• Cerebral vasoconstriction syndrome - a type of reflex syncope
• Neck tumour or swelling causing pressure on carotid sinus

Diagnosis

Measuring the postural blood pressure, although omitted from the physical examination in over half of patients with syncope, is the the part of the evaluation most likely to affect diagnosis or management.^[2]

Symptoms

• Loss of consciousness
• Sudden loss of balance
• Unexplained fall/collapse

Differential Diagnosis

Although syncope is not in itself a diagnosis, the following conditions may cause confusion leading to inappropriate management or visa versa:

• Explained falls (beware of patient's retrospective explaination)
• Hypoglycaemia
• Intoxication
• Sleep apnoea
• Neurological Conditions
  • Transient ischaemic attacks (TIA) of carotid origin but this does not cause syncope like symptoms !
  • Vertebro-basilar transient ischaemic attack
  • Epilepsy
  • Narcolepsy
  • Drop attacks
• Psychogenic pseudosyncope

Features

History

With vasovagal syncope, there is usually a prodrome of dizziness, nausea, tunnel vision and pallor. Such symptoms may have occurred previously without progressing to syncope. The trigger is usually standing up after a prolonged period of sitting/lying, but it can also occur with prolonged sitting. A complete and verified history from independent sources is necessary for accurate diagnosis. It has been shown that unexplained falls in the elderly are often caused by syncope, emphasising that patients can fail to recognise syncope or its prodrome. There may or may not be loss of consciousness. An anoxic seizure may follow immediately after the collapse, which is not epileptic (an EEG would show flattening rather than spikes/waves), and tends to be characterized by stiffening, posturing and fine twitching lasting a few seconds only. Warning signs in the history suggesting something more sinister include:

• Chest pain
• Syncope during exercise
• Syncope while supine
• Family history of sudden death in young person
• Odd history
• Unusual age group ie young child or new onset late in life

Syncope can be polyfactorial. The incidental hint of major surgery a few weeks before symptoms started can lead to the diagnosis of multiple pulmonary emboli, as can the more common change in drug therapy a few days before symptoms started.

Specific questions for systems review

• New pain, unpleasant sight, sound, smell or situation - vaso-vagal syncope
• Nausea, vomiting associated with syncope - vaso-vagal syncope
• Family history - vaso-vagal syncope
• Just after standing - orthostatic hypotension
  • Standing for prolonged periods - orthostatic hypotension
  • Standing in crowded, hot places - vaso-vagal syncope
• Relationship to change in drug therapy - orthostatic hypotension, cardiac arrhythmias, aortic stenosis or HOCM
• After/during a meal - post-prandial syncope
• On head rotation, pressure on neck from tumours, shaving, tight collars - carotid sinus syncope
• After exertion, isometric exercise - arrhythmias, structural heart disease, situational syncope
• Diabetes with neuropathy or atypical parkinsonism - orthostatic hypotension from autonomic neuropathy
• Palpitations before - arrhythmia
• Family history sudden death - arrhythmia
• Arm exercise - steal syndrome

Examination

Emphasize the cardiovascular examination looking at rate, rhythm and character of the pulse and the presence or absence of murmurs, heave and peripheral pulses but do not neglect the neurological or abdominal exam (pelvic tumour impairing venous return). Orthostatic blood pressure measurements should be done and affect diagnosis in about quarter of cases in emergency departments^[2]. If there is evidence of structural heart disease consider cardiac syncope.

Investigations

This is a condition in which it may be particularly tempting to order costly tests that will add little or nothing to the management. One study demonstrated massive resource waste in inappropriate electroencephalography, CT scans, and cardiac enzymes tests^[2]

• Do an ECG, which is cheap and non-invasive. Possible findings include:
  • Sinus bradycardia (<50 bpm), > 3 second pause, Mobitz type 1 second degree a-v block, sinoatrial block
  • Bifascicular block or other intraventricular conduction abnormalities (QRS duration greater than 0.12 s)
  • Pre-excitation (delta waves)
  • Prolonged QT interval
  • Changes suggesting acute myocardial infarction

Note the above is not exhaustive, but rare conditions such as Brugada syndrome and arrhythmogenic right ventricular dysplasia will have ECGs that meet the above descriptions.

A normal ECG and physical examination define a good prognosis group in terms of mortality. Some would feel that clear vasovagal syncope might not even require an ECG, and certainly does not require further investigation. Other initial investigations would be guided by clinical presentation and indeed should be based mainly on the need from the particular presentation to exclude non-syncope causes of loss of consciousness. Glucose (to exclude hypoglycaemia), electrolytes, and arguably a full blood count (to exclude anaemia).

• A suspicion of paroxysmal tachyarrhythmia should lead to prolonged ECG monitoring, with or without event recording.
• Exertion related symptoms should be investigated with an exercise test.
• If and only if there is evidence for structural heart disease should an echocardiogram be obtained.
• Tilt table studies should be done on those with recurrent syncope and a normal ECG, particularly where there is suspicion of neurally mediated symptoms.

Where symptoms are induced without changes in heart rate and blood pressure, then simultaneous EEG or cerebral blood flow monitoring may give the diagnosis of cerebral vasoconstriction syndrome.

• Carotid sinus massage should be done on the elderly or those where neck movements could have been associated with syncope. This may be combined with the tilt table study most effectively, but is likely to be contraindicated in those with evidence of carotid territory cerebrovascular disease.

Iron deficiency with/without anaemia is associated with neurocardiogenic syncope, though it is not yet proven that iron supplementation helps ^[3].

Treatment

Education

Patients and relatives need a full and reassuring explanation of vasovagal syncope with its usually benign prognosis.

The removal of addressable precipitants is always the first step. This includes :

• Advice on tight collars and scarves with carotid sinus syncope
• Fluid and salt intake should be optimized.

There are manoeuvres that can be employed when standing such as crossing legs, folding arms, shifting weight from heels to toes and back if periods of prolonged standing cannot be avoided.

Drug therapy

There is little good quality evidence to guide therapy. There is likely to be significant placebo effect.

• Midodrine.
• Betablockers, although widely used do not have a strong evidence base for effectiveness.
• Plasma expanders such as fludrocortisone and non-steroidal anti-inflammatory drugs can work with orthostatic hypotension

Pacing

• Pacing should be considered for heartblock less than 40/min or asystole lasting 3 seconds generally. However it will not prevent baroreceptor mediated syncope and the evidence base is not strong when patients have demonstratable mixed components to their syncope.

References

1. ↑ 2004 European Society of Cardiology Guidelines on Management (Diagnosis and Treatment) of Syncope.
2. ↑ ^{2.0 2.1 2.2} Mendu, Mallika L et. al. "Yield of diagnostic tests in evaluating syncopal episodes in older patients." Archives of internal medicine 169 (2009): 1299-305 - Abstract
3. ↑ Jarjour, Imad T, and Laila K Jarjour. "Low iron storage in children and adolescents with neurally mediated syncope." The Journal of pediatrics 153 (2008): 40-4 - Abstract