Vasovagal Faints and Cardiac Syncope

Vasovagal faints and cardiac disorders can result in loss of consciousness (syncope) or almost loss of consciousness (presyncope) as a result of cerebral hypoperfusion. Syncope can be trivial or, less commonly, life-threatening. Often making a diagnosis in syncope can be challenging, just as can be the management.

Some definitions:¹

• Collapse - abrupt loss of postural tone (with or without transient loss of consciousness)
• Syncope - transient loss of consciousness which results from global impairment of cerebral perfusion

The various types of syncope have various causes.

Neurally mediated syncope²

• Neurally mediated syncope (NMS) is also called reflex syncope, V VS, neurocardiogenic syncope, vasodepressor syncope, reflex anoxic/asystolic syncope (causes the common faint)
• Trigger required which results in a reflex response
• The response involves two elements:
  • Vasodilatation
  • Bradycardia
• These result in systemic hypotension and cerebral hypoperfusion (extent of each varies between individuals)
• Further classified according to trigger events, e.g:
  • Classical V VS - emotional stress is an example
  • Carotid sinus syncope - syncope follows mechanical stimulation of the carotid sinus, e.g. shaving
  • Situational syncope - associated with specific situations, e.g. coughing, micturition
  • Non-classical syncope - no clear trigger and a diagnosis of exclusion; however, patients have a positive response to tilt testing and carotid sinus massage

Orthostatic hypotension²

• Also called postural hypotension
• Occurs when arterial hypotension develops with changes in posture
• Most commonly occurs when standing up from a lying position; however, can also occur when sitting up from a lying position
• This results from failure of the autonomic nervous system, medications (e.g. anti-hypertensives) or hypovolaemia³

Cardiac arrhythmias

• All cardiac arrhythmias can lead to syncope or presyncope. However, the more serious types include VT and torsades de pointes.

Structural heart disease

• Structural abnormalities of the heart lead to syncope, as the heart cannot increase or maintain an adequate cardiac output when demands are placed upon it. Examples include aortic stenosis and hypertrophic obstructive cardiomyopathy (HOCM).

Psychogenic syncope

• This may be factitious
• Younger adults or teenagers
• Numerous attacks - perhaps several times per day compared with three or four a year in NMS
• Symptoms are often vague, and typical features of V VS, such as pallor and sweatiness, are absent
• There is often underlying anxiety, e.g. performance at school
• Attacks may be induced on a tilt table, but there is no change in heart rate or blood pressure and during the syncope the electrocardiogram (ECG) is unchanged

The lifetime risk for neurally mediated syncope is 50% for females and 25% for males.⁴ This is the usual diagnosis in young patients. On the other hand, in the elderly, cardiac causes, orthostatic and postprandial hypotension, and the effects of medications are common.⁴

Using the European Society of Cardiology guidelines on syncope, one study reported a definite diagnosis of the cause of syncope in 98% of patients, of which NMS accounted for the majority (~60%), orthostatic hypotension occurred in 10% and there were cardiac causes in 17%.⁵

A thorough history and examination may be all that is required to determine the cause of syncope. The following should be included in the initial evaluation:²

1. Is this true syncope?
2. Is cardiac disease present?
3. Are there any features in the history alone which help to identify the cause?

Features in the history which may help identify the cause

• Duration of syncopal attacks - years is more likely to represent NMS
• Trigger factors, e.g. emotion, heat, suggest classical V VS
• What was the patient doing at the time of event? For example, syncope on exercise suggests cardiac cause
• Classical V VS is usually sudden with a prodromal stage and with weakness, nausea, sweating, pallor, visual disturbance, abdominal discomfort, headache, pins-and-needles, light-headedness or vertigo
• Micturition related syncope - suggests situational syncope
• Coat hanger pain - is caused by hypoxia of tonic muscles in the neck and shoulder girdle in orthostatic hypotension
• Medications - may lead to postural hypotension in susceptible individuals
• Diabetes mellitus - associated with autonomic neuropathy
• Palpitations and chest pain suggest a cardiac cause
• Family history of sudden death should also raise the possibility of a cardiac cause
• Collateral history, if available, is crucial⁶

Features in the examination which may help identify the cause

• Orthostatic hypotension - postural decrease in systolic pressure >20 mmHg and/or diastolic pressure >10 mmHg or diastolic BP <90 mmHg with syncope or presyncope
• Cardiovascular examination may reveal a cardiac murmur in aortic stenosis

Initial investigations to perform to help identify the cause of syncope

Also see Investigations below.

• ECG - may reveal conduction defects, ischaemia, arrhythmias
• When evaluating the ECG look specifically for bradycardia, bifascicular or trifascicular block and pauses

Syncope is not only related to cerebral hypoperfusion, e.g. convulsions, hypoglycaemia, drug intoxication. In some other conditions consciousness is not truly lost, e.g. falls, drop attacks, psychogenic pseudo-syncope.

Use the initial history, examination and 12-lead ECG to guide you as to which tests to perform next. The tests that can be performed include:

• FBC - remember acute anaemia will cause syncope, as in chronic anaemias patients will adapt accordingly
• Blood glucose
• Echocardiography
• Exercise stress testing
• 24-hour Holter monitoring
• Prolonged ECG monitoring, including loop recorder
• CT brain scan
• Electroencephalogram - if convulsions are suspected, although of little use in unselected patients with syncope

If the cause of syncope still remains unclear then further tests might include:

• Tilt testing
• Carotid sinus massage with ECG monitoring
• Implantable loop recorder

Tilt testing and carotid sinus massage will detect NMS and should only be considered in patients in whom syncope is recurrent and severe. If the cause still remains unclear then repeat evaluation with repeat investigations may be required.² Patients may also require specialist input and may need admission to hospital for further management.

• The test is performed in a quiet warm room especially equipped for the purpose
• Patient lies flat on the table and is attached to real-time ECG and a blood pressure monitor
• After a short time the table is tilted head up to 60° or 70° and the position maintained for 40 minutes, or until typical symptoms occur
• 50%-60% of patients with unexplained syncope get their symptoms at around 20 minutes
• There is often dramatic slowing of the heart rate, or even ventricular arrest with a precipitous fall in blood pressure
• Leveling the table quickly restores the heart rate and blood pressure to normal and corrects the symptoms
• The sensitivity of the test may be increased by administering glyceryl trinitrate (GTN) sublingually after 20 minutes of being upright
• If syncope is reproduced in the absence of heart disease it is diagnostic, although false positives do occur⁷
• Syncope is much more frequent when GTN is used and so it is important to demonstrate bradycardia at the point of syncope to establish NMS
• GTN should not be used in aortic stenosis, HOCM, mitral stenosis, constrictive pericarditis, pulmonary hypertension, anaemia or hypovolaemia - all of which should have already been tested or looked for

Several studies have tried to produce scoring systems for syncope which attribute mortality risk according to the presence or absence of certain factors.
Presence of the following risk factors is associated with increased mortality at one year:⁸

• Abnormal ECG (not sinus bradycardia or sinus tachycardia, nor non-specific ST/T wave changes)
• Older than 45 years
• History of ventricular arrhythmias or congestive cardiac failure

Presence of two or more factors is associated with over 16% mortality

This depends on the cause - thus making a diagnosis necessary before advising and treating patients.

Neurally mediated syncope

• Reassurance and education is usually all that is required.
• Avoid potential triggers likely to induce syncope, e.g. prolonged standing in a hot environment or having a long hot bath.
• Take action at the first warning sign of collapse. If it is imminent, lie down flat with legs up on a chair or against a wall or sit down with head between the knees. Squatting down on the heels can be very effective and is less noticeable in public. These techniques help move venous blood that has pooled in the limbs, aiding circulation to the brain. When feeling better, get up carefully. If symptoms return, resume the position.
• However, if syncope is very frequent, the patient is at risk of injury, as attacks are unpredictable or, if syncope occurs during high-risk activities such as driving, then treatment may be required.
• However treatment options are limited and include:
  • Tilt training - prolonged periods of upright posture; requires good compliance, as several sessions are needed and deconditioning occurs quickly on stopping.²
  • Isometric counterpressure manoeuvres, e.g. leg crossing or arm tensing which can increase blood pressure enough to prevent syncope.
  • Medications - various medications have been used, e.g. beta blockers, clonidine, fludrocortisone; however, large randomised controlled trials have failed to show any conclusive benefits of these measures.²
  • Cardiac pacing (dual chamber preferred) - like drugs in V VS, does not also appear to have any major benefit, although this may depend on the patients selected for it. Despite this, it may be useful in carotid sinus syncope.

Orthostatic hypotension

• Stop any offending drugs
• Avoid alcohol
• In some patients the above may not be enough and the following may be useful:
  • Encourage oral fluid intake
  • Low dose of fludrocortisone
  • Raising head of bed
  • Support stockings to reduce pooling of vascular volume
  • Leg crossing and arm tensing as above
  • Drugs that increase total peripheral resistance, e.g. midodrine, an alpha-1 adrenergic agonist (available in UK on a named patient basis only)

Cardiac cause of syncope

• Treatment is aimed at the underlying cause, e.g. anti-arrhythmics, pacing, implantable cardiac defibrillators
• Electrophysiological studies and ablation may also be required for arrhythmias
• Treatment of structural disorders of the heart are again aimed at the underlying cause

Having a syncopal attack may lead patients to injure themselves. This may be trivial but, in the elderly, extradural or cerebral haemorrhages can be the result. Before a diagnosis is reached, patients should be advised about taking safety precautions, e.g. not closing the door whilst bathing, as there is a risk of drowning.

Prognosis varies according to the underlying cause. The all-cause mortality in subjects with reflex syncope is not higher than in the general population.⁴

Driving is not a problem for a simple faint but greater restrictions apply if the situation is more complicated or if diagnosis is less clear. If in doubt, contact the Driver and Vehicle Licensing Agency (DVLA). They do not have to be informed of a simple faint but failure to notify other conditions can lead to a fine.

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