Syncope is very common and will affect 42% of people during their lifetime (NICE guidance). Whilst some syncopal episodes cause limited harm, others cause significant debility, or herald severe illness or sudden death. Furthermore, misdiagnosis is common and therapeutic opportunities are missed.

This toolkit will guide the GP through the initial assessment, appropriate investigation and management of patients with syncope and orthostatic intolerance (presyncope symptoms). It will increase practitioner confidence in diagnosis, awareness of key indicators and red-flags, and enable timely signposting of patients towards life-improving or life-saving care.

"The only difference between syncope and sudden death is that in one you wake up" - George Engel

Syncope key facts

Why is syncope important?

• Syncope is common and occurs in 42% of people by the age of 70
• Health related quality of life is poor in people with recurrent vasovagal syncope
• After attending A&E with syncope, 0.7% of patients die in the next 7-30 days, and 10% within a year - mortality is highest in those with cardiac syncope.
• GPs often omit screening for the red flags in syncope that help to detect cardiac syncope
• Misdiagnosis affects up to 30% of patients with epilepsy; cardiovascular syncope is the most common misdiagnosis in epilepsy
• Syncope presents to the GP or A&E six times more often than epilepsy
• Syncope is an under-recognised cause of recurrent falls and older patients commonly experience amnesia for events before the syncope or fall
• Cardiovascular events cause 45% of unexplained falls in people with dementia
• Orthostatic intolerance syndromes (mainly due to orthostatic hypotension and postural tachycardia syndrome) cause chronic debility in the young and old.

Patient information

• STARS (Syncope Trust and Reflex anoxic Seizures) -  includes blackouts checklist, booklet, factsheets and patient information videos
• Stop Fainting
• Dysautonomia International.

Credits

Authors

• Prof Lesley Kavi (Syncope Clinical Champion)
• Dr Harjeevan Gill (Syncope Clinical Fellow)
• Dr Morwenna Opie-Moran
• Dr Nick Gall

Reviewers

• Prof Richard Sutton
• Prof Robert Sheldon
• Prof Rose Anne Kenny
• Prof William Whitehouse
• Mrs Trudie Lobban MBE and STARS team
• Dr Dharini Shanmugabavan
• Dr Jit Solanki
• Dr James White
• Prof Catherine Nelson-Piercy

Images

• Prof  Wouter Wieling
• Dr Dean Jenkins
• Dr Alexander Breitenstein
• Syncope Unit at Hammersmith Hospital

Funding

Medtronic unrestricted educational grant

References

Download Syncope toolkit references (19 KB PDF)

Definitions and causes of syncope and blackouts

Syncope and blackouts are both symptoms, and not a diagnosis in their own right. It is therefore important to establish the underlying causes. Syncope does not have the same meaning as blackouts.

In this section:

• Definitions
• Causes of blackout
• Mechanisms of syncope

Definitions

Blackout is also known as Transient Loss of Consciousness (TLoC).

TLoC is defined as a state of real or apparent loss of consciousness with loss of awareness, characterised by abnormal motor control, loss of responsiveness, and a short duration.

Syncope is a subset of blackouts and is defined as TLOC due to cerebral hypoperfusion, characterised by a rapid onset, short duration, and spontaneous complete recovery. Syncope occurs when cerebral blood flow ceases for 6-8 seconds or there is a drop in systolic blood pressure below 60mmHg, and typically lasts for under one minute.

Presyncope describes the symptoms and signs that occur before losing consciousness. From studies in A&E, presyncope should be managed as for syncope as the prognosis is the same.

Orthostatic intolerance is a heterogeneous condition in which the standing position provokes a variety of symptoms such as dizziness, discomfort, nausea, and palpitations.

Causes of blackouts

Diagram key:

• PPS - ‘psychogenic’ pseudo-syncope
• NES - non-epileptic seizures
• TIA - transient ischaemic attack
• SAH - subarachnoid haemorrhage
• 1y - primary
• 2y - secondary

Download causes of blackout diagram (89 KB PPT)

Mechanisms of syncope

Syncope is caused by a reduction in cerebral blood flow due to a drop in blood pressure. A fall in systolic blood pressure to below 60mmHg with or without a pause in heart rate of 6-8 seconds will usually cause syncope.

Blood pressure is the product of cardiac output and peripheral resistance, and a reduction in either can cause syncope.

Reduced cardiac output may be due to arrhythmia (bradycardia or tachycardia), structural disease, reduced cardiac contractility or reduced venous return to the heart and volume depletion.

Reduced peripheral resistance can result from failure to vasoconstrict or inappropriate vasodilatation.

Often more than one mechanism is present when syncope occurs.

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Vasovagal syncope

In this section:

• Reflex syncope (also called neurally mediated syncope)
• Types of reflex syncope
• Vasovagal syncope in younger children
• Vasovagal case histories
  

Reflex syncope (also called neurally mediated syncope)

There are primarily two mechanisms of reflex syncope:

• Vasodepression - insufficient sympathetic tone resulting in dilation of blood vessels leading to pooling of blood in the splanchnic bed, pelvis and lower limbs. This reduces venous return and stroke volume, ultimately causing hypotension. This is the ‘vaso’ part of vasovagal.
• Cardioinhibition - occurs later than vasodepression and less frequently in the older patient. It presents as increased parasympathetic tone causing bradycardia or asystole. This is the ‘vagal’ part of vasovagal.

Types of reflex syncope

Vasovagal

• Orthostatic vasovagal syncope - can occur when standing (although 10% of vasovagal syncope episodes occur in people when sitting or rarely when supine)
• Emotional - can occur with pain, medical instrumentation, sight of blood or needles.

Reflex syncope is more likely to occur when several risk factors or triggers occur at the same time. Patients typically experience activation of the autonomic nervous system resulting in sweating, flushing, pallor, and palpitations, and reduced blood pressure that reduces cerebral perfusion. This can result in light-headedness and altered vision and hearing. Symptoms rapidly improve upon assuming a horizontal position.

Reflex syncope is the most common type of syncope presenting to GPs. Patients often describe a family history of vasovagal syncope.

There are two peaks in incidence of vasovagal syncope, one in adolescents, a little more common in females and a second in older age, a little more common in males. Episodes often occur in clusters and then improve for reasons that are not well understood. Patients who experience frequent episodes have a significantly reduced quality of life.

Management of reflex syncope

Situational syncope

• Micturition, defaecation, swallowing, cough, sneeze, laughing, trumpet blowing
• Post-exercise.

Carotid sinus syndrome (CSS)

• Carotid sinus hypersensitivity (CSH) – when a hypersensitive carotid sinus is stimulated by cartoid sinus massage (CSM), in an asymptomatic patient, causing a ventricular pause of over three seconds, and/or drop in blood pressure of over 50 mmHg.

• Carotid sinus syndrome (CSS) is CSM causing syncope in a patient with a history of syncope and symptom reproduction.

CSS usually occurs in older men with pre-existing cardiovascular disease. CSS is diagnosed by history and carotid sinus massage. This should be undertaken upright and supine in a specialist unit with beat to beat recording of heart rate and blood pressure.

Vasovagal syncope in younger children

Vasovagal syncope in younger children, also called reflex anoxic seizures (RAS), infantile reflex syncopal attacks or pallid breath-holding spells. RAS and pallid breath-holding spells are confusing terms as these episodes do not involve breath-holding or seizures.

Following an unpleasant stimulus, the child loses consciousness due to cardio-inhibitory vasovagal syncope. Care must be taken to differentiate this from structural or electrical cardiac pathology by history, examination and ECG and referral to a paediatrician may be indicated. Management of RAS is usually explanation and reassurance as it always resolves, and pacing should generally be avoided unless extremely incapacitating.

Support for parents can be obtained from the Syncope Trust And Reflex anoxic Seizures (STARS).

Vasovagal case histories

• Carotid sinus syndrome (CSS)
• Convulsive syncope
• Vasovagal Syncope affecting employment
• Post-exercise induced neurally-mediated syncope

Case histories - Vasovagal syncope

• Carotid sinus syndrome (CSS)
• Convulsive syncope
• Vasovagal syncope affecting employment
• Post-exercise induced neurally-mediated syncope

Carotid sinus syndrome (CSS)

History

A 68 year old gentleman presents to you with episodes of recurrent syncope. He describes the episodes as occurring when washing and shaving in the morning. His syncope was briefly preceded by dizziness, and he denies any other warning symptoms. He has a history of anxiety for which he takes sertraline 50 mg once daily. He is an ex smoker of 20 pack years.

Examination

He is normotensive with no postural drop between lying and standing blood pressures. Cardiovascular examination is normal.

Which investigations should be performed in primary care?

The key investigation in this case is an ECG to identify any underlying cardiac abnormality that may be linked to the patient's symptoms. The ECG for this patient is normal.

What would you do next?

This patient has unexplained syncope and you should advise him that he must not drive and that he must notify the DVLA. The next step would be to refer to a specialist for further investigation of this patient's syncope. A referral to a cardiologist or syncope clinic would be most appropriate.

Outcome

This patient is reviewed by a cardiologist. Carotid sinus massage is performed with the patient upright and with beat to beat heart rate and blood pressure monitoring. The patient reports dizziness then faints with an associated ventricular pause of 9 seconds noted on his monitor. He is referred for pacemaker insertion and subsequently has no further episodes.

Learning points

• Carotid sinus syndrome (CSS) should be considered in all older patients presenting with syncope with normal examination and normal or near-normal ECG
• Triggers for CSS include head rotation or pressure on carotid sinus - which may be caused by tumours, shaving, or tight collars
• Carotid sinus massage of 10 seconds causing syncope associated with asystole for over 3 seconds and/or a fall in systolic blood pressure of more than 50 mm Hg is diagnostic of CSS.
• If initially negative in the supine position, carotid sinus massage should be performed during passive upright tilting as 30% of cases are missed by testing in the supine position alone.

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Convulsive syncope

History

A 58 year old gentleman consults with his GP with a 2 year history of funny turns. He describes episodes of buzzing in his ears associated with feeling dizzy, but no loss of consciousness.

Examination

He is normotensive with no postural drop between lying and standing blood pressures. Cardiovascular and ear, nose and throat examination are normal.

Which investigations were performed in primary care?

A hearing test is organised due to the recent history of tinnitus. In this case the hearing test is normal.

What happened next?

The patent is referred to an ENT specialist for further investigation of the tinnitus and dizziness. An MRI of his internal acoustic meatuses is requested, and this is normal. He is diagnosed with vestibular migraines and treatment with beta-blockers is commenced.

He consults 4 months later after experiencing another episode, which is witnessed by his wife. He reports having felt dizzy, hearing buzzing in his ears, falling down and his wife corroborates that he was unconscious and developed jerking movements of his arms for approximately 10 seconds before stopping. He regained consciousness after approximately 30 seconds and was not confused but reported feeling tired and slow. There was no associated incontinence or tongue biting.

What would you do next?

This history raised the possibility of a seizure. He consults his GP and is advised not to drive and to notify the DVLA. He is referred to a neurologist for further assessment. They organise an EEG which is normal, diagnose epilepsy and commenced treatment with carbamazepine. Over the next 3 months he continues to have similar episodes approximately once a month, despite increases in his carbamazepine dose and monitoring showing therapeutic drug levels.

Frustrated with his continuing symptoms he consults with you for a second opinion.

What could you do next?

You review his medications, stop his beta blocker and organise an ECG which is normal. As he is experiencing recurrent syncopal blackouts, despite escalating anticonvulsant therapy, you refer him to the local syncope clinic for further evaluation.

Outcome

In the syncope clinic, he undergoes further investigations including 24-hour Holter monitoring and carotid sinus massage tests which are normal. Tilt table testing reveals sudden and prolonged bradycardia after 17 minutes, resulting in loss of consciousness associated with asymmetrical mild limb jerking movements. He feels dizzy and experiences buzzing in his ears before fainting. The diagnosis is asystolic vasovagal syncope. He is provided with self-management advice including physical counterpressure manoeuvres to prevent syncope, information about increased fluid and salt intake and avoiding triggers. This fails to improve his symptoms, and he is later successfully treated with a dual chamber pacemaker.

Learning points

• Syncope causes transient cerebral ischaemia which may lead to myoclonic jerks. Jerks often begin after several secdonds after loss of consciousness and not immediately as in epilepsy
• Syncope tends to be associated with a shorter duration of loss of consciousness and rapid recovery with little or no confusion compared with epilepsy
• 24-hour Holter monitors are an unhelpful investigation unless episodes occur very frequently (ideally daily).
• In vasovagal syncope (and also in carotid sinus syndrome) cardiac pacing can be effective if the cardioinhibitory reflex is dominant; there is no role for pacing in the preventing hypotension due to vasodilatation
  

• Differentiating vasovagal syncope epilepsy and epilepsy

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Vasovagal Syncope affecting employment

History

A 29 year old security guard consults with you after developing episodes of syncope associated with prolonged standing during guard duties, especially on warm days. These are associated with nausea and sweating prior to syncope. Witnesses report no seizure activity. He has no significant past medical history and takes no medications.

Examination

Cardiovascular examination is normal with no postural drop in blood pressures.

Which investigations should be performed in primary care?

An ECG performed in the surgery is normal.

What would you do next?

There is a clear history of neurocardiogenic (vasovagal) syncope triggered by prolonged standing. He should be provided with advice about preventing syncope by increasing fluids, salt, physical counterpressure manoeuvres and avoiding excessive heat. However, his episodes continued, and he was referred to a syncope service for further assessment. He was advised that he could continue to drive as syncope only occurred after prolonged standing.

Outcome

He undergoes tilt table testing and after 8 minutes of head up tilt he reports feeling nauseated, begins to sweat profusely and develops a bradycardia with a profound drop in blood pressure. He loses consciousness and subsequently regains consciousness when lowered to the supine position.

The patient's symptoms were reproduced exactly during the tilt table test and therefore a diagnosis of vasovagal syncope is confirmed. As his syncopal episodes continue despite lifestyle measures, he commences treatment with fludrocortisone and later midodrine. Although syncope occurred less frequently, ultimately it was necessary to change his employment duties.

Learning points

• Vasovagal syncope reproduced on tilt table testing can demonstrate either cardioinhibitory, vasodepressor or mixed responses
• Recurrent vasovagal syncope in patients may have consequences for their occupation
• Self-management advice, medication and psychosocial support may be helpful
• If vasovagal syncope only occurs with prolonged standing, group 1 vehicle drivers may continue to drive, but group 2 vehicle divers (bus and lorry) must cease driving immediately and notify the DVLA.

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Post-exercise induced neurally-mediated syncope

History

A 22 year old female university student on the rowing team seeks advice from you after developing episodes of syncope following training on a rowing machine. She also experienced episodes of presyncope after rowing whilst still seated in the rowing boat. She has no significant past medical history and is not taking any regular medications. The syncope episodes were witnessed by her teammates and occurred after completing her exercises with loss of consciousness lasting between 10 and 30 seconds. She complained of feeling generally unwell after the episodes.

Examination

Cardiovascular and neurological examination is normal with no postural drop between lying and standing blood pressures.

Which investigations should be performed in primary care?

An ECG is the most useful initial test to perform and her ECG is normal.

What happened next?

Syncope during exercise is a red flag for a cardiac cause; syncope after exercise is usually associated with less severe outcomes.  In view of the episodes while seated and high-risk syncope (alone in a rowing boat on water), she is referred for further specialist assessment via a syncope clinic and is advised not to drive until she had undergone further assessment.

Outcome

At the syncope clinic she undergoes further testing and has a normal echocardiogram. Exercise testing is performed and after exercise she is found to develop a significant drop in blood pressure and heart rate and experiences marked presyncope; blood pressure recovers quickly after lying supine. The test is repeated, but this time she is asked to actively cool down after the test and the symptoms do not recur. She is diagnosed with post-exercise induced vasovagal syncope. She can be advised that she can return to driving after 4 weeks.

Learning points

• Syncope after exercise is typically vasovagal in origin and benign in contrast to syncope during exercise, which is most likely to be arrhythmic in origin and not benign
• Syncope related to exercise can herald a potentially fatal underlying cardiac condition and requires thorough investigation.

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Orthostatic hypotension

Orthostatic hypotension is the mechanism of syncope in around 10% of patients.

In this section:

• Definitions
• Symptoms of orthostatic hypotension
• Causes of orthostatic hypotension
• Case history - Orthostatic hypotension and autonomic neuropathy
• Case history - Orthostatic hypotension after squatting

Definitions

Classical OH: a progressive and sustained fall in systolic blood pressure from baseline value greater than or equal to 20 mmHg or diastolic blood pressure greater than or equal to 10 mmHg, or a decrease in systolic blood pressure to less than 90 mmHg which usually occurs within three minutes of standing.

Initial postural hypotension (head rush): blood pressure decrease on standing of more than 40 mmHg systolic blood pressure usually with more than 20 mmHg drop in diastolic blood pressure within 15 seconds of standing. This is a common cause of syncope in young people.

Delayed postural hypotension: blood pressure fall occurs after three minutes (and may occur more than 10 minutes after standing). This is common in the elderly.

Note that the definition of orthostatic hypotension does not state whether the fall in blood pressure should or should not be accompanied by symptoms.

Some patients with chronic orthostatic hypotension can remain conscious despite extraordinarily low blood pressure due to effective cerebral autoregulation.

Orthostatic hypotension can be a chronic, debilitating illness that is associated with reduced quality of life, risk of falls, cognitive impairment and increased mortality. It is common and affects up to 20% of older people living at home and almost one in four older people in long-term care.

Symptoms of orthostatic hypotension

Symptoms include:

• Light-headedness
• Difficulty thinking
• Orthostatic headache
• Fatigue, weakness
• Nausea
• Visual and hearing disturbances (such as black or white dots, greying out, temporary loss of vision, ringing or rushing sounds)
• Posterior neck discomfort (coat hanger pain)
• Syncope
• Recurrent unexplained falls.

Exacerbating factors:

• Standing
• More severe in the morning
• Worse immediately after exercise
• High environmental temperature
• After meals (post-prandial hypotension)
• After prolonged bedrest (deconditioning).

Relieving factors:

• Lying down
• Less severe or absent when sitting.

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Causes of orthostatic hypotension

See Management of orthostatic hypotension

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Orthostatic hypotension case histories

• Orthostatic hypotension and autonomic neuropathy
• Orthostatic hypotension after squatting case history

Case histories - Orthostatic hypotension

• Orthostatic hypotension and autonomic neuropathy
• Orthostatic hypotension after squatting case history

Orthostatic hypotension and autonomic neuropathy

History

A 60 year old gentleman presents to you with a 1 month history of dizziness when standing. He has also previously experienced 2 episodes of witnessed syncope lasting between 15 and 30 seconds with rapid recovery. There was no associated tongue biting, incontinence or limb jerking. He reports constipation, dry eyes and a dry mouth. He has no significant past medical history and is not taking any regular medications.

Examination

Cardiovascular examination is normal, and his lying blood pressure is 128/64 dropping to 84/44 on standing.

Which investigations should be performed in primary care?

Blood tests including U+E, FBC and random cortisol are useful in investigating orthostatic hypotension. An ECG performed in the surgery is normal.

What would you do next?

These features suggest orthostatic hypotension. You advise him of lifestyle measures to prevent postural hypotension including increased fluids, compression garments, postural counterpressure manouevres and sleeping with the head end of his bed raised. His symptoms continue and you prescribe fludrocortisone. You review him 4 weeks, but he reports no improvement in his symptoms, so you refer him to the local syncope clinic for further assessment.

Outcome

He undergoes autonomic testing which confirms autonomic dysfunction and after further assessment by a neurologist, he is diagnosed with an autoimmune autonomic neuropathy. He is treated with a combination of fludrocortisone and midodrine, and his symptoms improve.

Learning Points

• Most causes of orthostatic hypotension are due to side effects of medication or intravascular volume depletion; however, a small proportion are due to impairment of autonomic reflexes.
• Autonomic failure may be due to a primary cause (pure autonomic failure, multiple system atrophy, Parkinson's Disease) or secondary to other diseases (e.g. diabetes, amyloidosis).
• Consider these rarer causes if there are no obvious culprit drugs and a lack of response to treatments in primary care.

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Orthostatic hypotension after squatting case history

History

A 32 year old lady presents to her GP after experiencing an episode of syncope whilst exercising. She has recently started an aerobics class and after squatting then standing, she reports having felt light headed. She developed loss of consciousness for approximately 15 seconds and was not confused on recovery. The episode was witnessed by the other members of her class. She has no significant medical history and does not take any regular medications.

Examination

Cardiovascular examination is normal, with no postural difference in blood pressures.

Which investigations should be performed in primary care?

An ECG should be performed and this is normal.

What happened next?

Due to the association of syncope with exercise, the GP refers her to a cardiologist. for further assessment.

Outcome

The cardiologist monitors her blood pressure and heart rate with beat to beat monitoring whilst squatting and standing and her blood pressure is noted to drop when she stands up from squatting and she again reports feeling dizzy. She is diagnosed with initial or immediate orthostatic hypotension and advised to use physical counter-manoeuvres by tensing the muscles in her legs when standing from sitting or lying with no further syncopal episodes.

Learning points

• A detailed history is key when assessing syncope to determine triggers which may provide a clue to the underlying diagnosis.
• Standing from squatting may lead to a significant fall in blood pressure that can precipitate syncope due to sudden reduction of venous return.
• Physical counter-manoeuvres can counteract this effect by antagonising the blood pressure fall and increasing venous return from muscles. They are easily taught to patients.

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Postural tachycardia syndrome (PoTS)

Postural Tachycardia Syndrome (PoTS) was named and defined in 1993. Affected patients experience a persistent tachycardia on standing, associated with debilitating symptoms of orthostatic intolerance (most commonly light headedness, palpitations and fatigue). In the UK, up to 60% of patients describe syncope.

It is a heterogenous group of disorders that usually afflicts younger women. The pathophysiology of PoTS is not well understood; it seems likely that there are multiple aetiologies.

For more information about diagnosis and management of PoTS in primary care, see:

• PoTS on a Page for GPs
• A series of articles on PoTS published in Autonomic Neuroscience

Overlap between vasovagal syncope, orthostatic hypotension and PoTS

Further reading

• PoTS UK leaflets and resources
• A brief overview of PoTS for GPs – ‘PoTS on a page’ (PDF)
• Canadian Cardiovascular Society position statement on Postural orthostatic Tachycardia Syndrome (PoTS) and related disorders of chronic orthostatic intolerance
• An open access journal supplement explaining PoTS and its management in detail
• Videos of educational lectures and PowerPoint slides on PoTS for healthcare professionals.

Postural Tachycardia Syndrome (PoTS) case history

History

A 29 year old woman consults with you due to daily symptoms over the previous 12 months of pre syncope, fatigue and palpitations following a viral illness. She recalls 3 definite syncopal episodes and had attributed these to being dehydrated and therefore had not sought medical attention previously. These syncopal episodes appeared to occur after she had been standing for long periods of time as a retail worker. She has no significant past medical history and is not taking any medication.

Examination

Physical examination is normal and postural blood pressures showed no significant drop, but her heart rate increases from 82 bpm whilst sitting to 124 bpm when standing with associated light-headedness and fast palpitations.

Which investigations should be performed in primary care?

An ECG should be performed, and this is normal. She should also have U+E, TFTs, and an FBC. Consider a glandular fever screening test.

What would you do next?

The increase in her heart rate on standing raises the possibility of postural tachycardia syndrome (PoTS) and she should be referred to a local cardiologist with an interest in PoTS for further assessment.

Outcome

The cardiologist organises a 24-hour Holter monitor which shows sinus rhythm ranging from 62 bpm to 168 bpm; the recurrent tachycardias relate to periods of activity during the day.

She undergoes a tilt table test which reveals a persistent increase in her heart rate from 75 bpm to 125 bpm on passive tilting. Nitroglycerin is administered which shows a further rise in heart rate followed by a fall in blood pressure and an asystolic pause associated with syncope. She is diagnosed with postural tachycardia syndrome and vasovagal syncope. She starts treatment with advice on fluid and salt intake and gentle supine exercise. Later fludrocortisone is added with good symptom control when she was followed up.

Learning points

• PoTS is characterised by chronic symptoms including light headedness, weakness, palpitations and fatigue especially when upright
• There is a persistent increase in heart rate of over 30 bpm from supine to the upright position without a reciprocal fall in blood pressure.
• Some patients have episodes of vasovagal syncope, but its incidence is similar to that of the general population.
• Stand test can diagnose PoTS and a tilt table test is useful in patients with an unclear cause for their symptoms.
• Secondary care clinicians with an interest in PoTS may be found in cardiology, neurology, medicine for the elderly and paediatric departments. In some areas of the UK there are no specialists available and out of area referrals may be necessary, especially for complex patients.

Cardiac syncope

Approximately 9% of patients presenting with syncope were found to have an identifiable cardiac cause.

In this section:

• Cardiac syncope and mortality
• Cardiac arrhythmias
• Arrhythmia caused by medication (long QT interval)
• Structural heart disease
• Other cardiovascular syncope
• Cardiac syncope case histories.

Cardiac syncope and mortality

The mortality associated with syncope is highest when the episode has a cardiac cause and therefore it is important not to assume that a faint is vasovagal in nature without appropriate assessment.

In general, when heart conditions cause syncope, the cause is usually:

• Structural heart disease in older people
• Rarer genetic cardiac conditions in the young.

Sudden death in young athletes is rare but has obvious devastating consequences and is discussed in more detail in our section about syncope in athletes. In comparison, there is no increased risk of death amongst people with vasovagal syncope.

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Cardiac Arrhythmias

Arrhythmias cause syncope due to reduced cardiac output.

Inherited disorders causing arrhythmia and syncope

Long QT syndrome (LQTS):

• Long QT syndrome is diagnosed if the corrected QT interval (QTc) is more than or equal to 480 ms (or QTc is more than or equal to 460 ms in the presence of syncope)
• Computerised ECG machine reporting of QT interval is generally accurate although this can over or under report
• 13 genetic mutations have been identified (LQTS types 1-13). Prevalence of the autosomal dominant form is 1 in 2500
• Jervell and Lange-Nielsen is a rare syndrome which causes profound congenital sensorineural hearing loss, syncope and sudden cardiac deaths due to LQTS.
• The mean age at presentation of LQTS is 14 years
• Triggers for arrhythmias can include exercise, fright, the post-partum period, and QT prolonging drugs
• The risk of sudden cardiac death is 0.9%, but this increases to 5% in people who experience syncope
• Beta blockers can reduce this risk, but an implantable cardioverter defibrillator (ICD) will be considered for those who continue to experience unexplained syncope despite beta blockers.

See an example of a long QT ECG on ECG Library. 

Short QT syndrome:

• Short QT syndrome is very rare, but highly lethal
• It can present in the first month of life (for examples as sudden infant death syndrome) and over 40% of patients experience cardiac arrest by the age of 40 years
• A short QT can be diagnosed if the QTc less than or equal to 340 ms or less than or equal to 360 ms if other risk factors are present.

Brugada syndrome:

• Patients with Brugada syndrome and syncope are more likely to have arrhythmic events such as VT and VF
• However non-arrhythmogenic syncope is at least as common in this group as in the general population and investigation with an implantable loop recorder may be indicated to determine whether an ICD would be recommended
• Some drugs can trigger arrhythmias in affected patients and more information including lists of offending medications can be found at BrugadaDrugs.org.

Congenital Accessory Pathways - Wolff-Parkinson-White syndrome (WPW):

• WPW can be asymptomatic, or present with syncope, presyncope or palpitations.
• Sudden death is very rare, and tends to occur during exercise
• Treatment is usually with catheter ablation
• Digoxin and calcium channel blockers diltiazem and verapamil should never be used in patients with WPW as this combination can provoke lethal ventricular arrhythmias See the British National Formulary (BNF)
• Atrial fibrillation in WPW is a worrying finding as this arrhythmia can degenerate into ventricular fibrillation.

Visit the British Heart Foundation to see more on Wolff-Parkinson-White Syndrome.

Visit ECG Library for examples of a Wolff-Parkinson-White syndrome ECG and a WPW with atrial fibrillation ECG.

Catecholaminergic polymorphic ventricular tachycardia (CPVT)

Visit the British Heart Foundation to see more on Catecholaminergic polymorphic ventricular tachycardia.

Bradycardias

Sinoatrial (SA) node disease

A variety of conditions where sinus arrest or SA block are seen on ECG to cause syncope. A pacemaker may be indicated.

Bradycardia-tachycardia syndrome

An example of this is a prolonged sinus node pause following self-termination of a tachycardia, resulting in syncope.

Atrioventricular (AV) node disease:

• 2nd degree block (Mobitz II), 3rd degree block (complete heart block)
• Pacing can be effective in preventing syncope in both types of AV block.

Bifascicular bundle branch block (right BBB plus left anterior or left posterior hemiblock or left BBB):

• Patients with bifascicular block and syncope are at risk of intermittent complete heart block and may benefit from a permanent pacemaker - a routine echocardiogram is worthwhile to see if these patients also have structural heart disease
• Patients with syncope, bifascicular block and a left ventricular ejection fraction less than 35% benefit from an implantable defibrillator as they are at risk of ventricular tachycardia and ventricular fibrillation.

Tachycardias

Paroxysmal SVT:

• AV nodal re-entrant tachycardia
• AV re-entrant tachycardia
• Atrial flutter - see example of atrial flutter ECG
• Ectopic atrial tachycardia.

All can be treated with ablation or anti-arrhythmic drugs.

Paroxysmal VT

In ventricular tachycardia with syncope, ablation, drug therapy or an implantable cardioverter defibrillator (ICD) may be indicated. Visit ECG Library for an example of a ventricular tachycardia ECG.

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Arrhythmia caused by medication (Long QT interval)

Medication can provoke a variety of brady- and tachyarrhythmias, for example beta blockers can cause sinus bradycardia. However, one that commonly causes concern for GPs is drug-induced long QT syndrome.

Torsades de pointes is a common form of ventricular tachycardia in this situation and can be due to medication that prolongs the QT interval. If it self-terminates it can cause syncope, but torsade de pointes can also progress to ventricular fibrillation and sudden death. This arrhythmia is more likely to occur in the presence of low potassium or magnesium levels.

Drugs that carry the greatest risk of prolonging the QT interval are selected antiarrhythmic drugs; however, other drugs including antipsychotics, antidepressants, antibiotics, and antihistamines are also culprits. Polypharmacy increases this risk.

Consulting room computer software or the British National Formulary app can assist in identifying drug interactions. A useful website is CredibleMeds.

Visit ECG Library for examples of a Toursade de Pointes ECG, ventricular tachycardia ECG and ventricular fibrillation ECG.

Management

Patient on QT prolonging drugs should be advised to report lightheadedness, palpitations or syncope.

If a QT prolonging medication results in a QTc interval of 470-500ms in men, or 480-500ms in women, the dose should be reduced, or the drug stopped. If the QTc is more than 500ms the medication should be reviewed urgently in association with their secondary care specialist, if appropriate and stopped if possible.

Repeat the ECG after reducing or stopping the offending medication. Details of drugs that prolong the QT interval can be found at CredibleMeds.

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Structural Heart Disease

Myocardial ischaemia and its structural cardiac complications

Syncope is almost twice as common in people with cardiovascular disease than those without.

In acute ischaemia, the mechanism can be vasovagal (especially in inferior MI), high grade AV block or tachyarrhythmias. During the first weeks after an acute ischaemic event, there is a higher risk of ventricular arrhythmia, and syncope following MI is particularly concerning.

Hypertrophic cardiomyopathy

Unexplained syncope predicts sudden death and ICD may be indicated. Visit the British Heart Foundation for more on hypertrophic cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Unexplained syncope suggests risk of arrhythmia and sudden death and ICD may be recommended. Visit the British Heart Foundation for more on arrhythmogenic right ventricular cardiomyopathy.

Aortic Stenosis

Syncope usually occurs during exercise in aortic stenosis due to inability to increase cardiac output to match demand and indicates a poor prognosis.

‘SAD’ symptoms are red flags indicating severe aortic stenosis and urgent referral to cardiology or admission to hospital should be considered.

Myotonic and Muscular dystrophies

Myocardial fibrosis and conduction abnormalities can occur. In type 1 myotonic dystrophy, sudden death was documented in 3.6% of affected patients.

Other structural heart disease:

• Cardiac mass (atrial myxoma, ball thrombus)
• Pericardial disease
• Pericardial tamponade
• Congenital abnormalities of the coronary arteries
• Prosthetic valve dysfunction.

Other cardiovascular syncope

Pulmonary embolism and pulmonary hypertension

These conditions effectively obstruct the circulation leading to underfilling of the left ventricle. In acute pulmonary embolism the right ventricle may dilate and have markedly reduced function.

Aortic dissection

This is a life-threatening condition which may cause syncope by several different mechanisms:

• Pain can lead to vasovagal syncope, but with incomplete recovery
• By obstructing the circulation
• By rupturing into the pericardium causing cardiac compression.

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Arrhythmia further reading

• Arrhythmia Alliance patient booklets
• The history of fainting from the Arrythmia Alliance is a short video about syncope and sudden cardiac death
• Ventricular Arrhythmias and the prevention of sudden cardiac seath - European Society of Cardiology guidelines 2015
• Management of patients with Supraventricular Tachycardia) - ESC clinical practice guidelines 2019.

Cardiac syncope case histories

• Drug induced bradycardia
• Hypertrophic obstructive cardiomyopathy
• Long QT syndrome
• Myocardial Ischaemia
• Pulmonary Embolism
• Aortic Stenosis
• Atrial fibrillation
• Brugada syndrome

Case histories - Cardiac syncope

• Drug induced bradycardia
• Hypertrophic obstructive cardiomyopathy
• Long QT syndrome
• Myocardial Ischaemia
• Pulmonary Embolism
• Aortic Stenosis
• Atrial fibrillation
• Brugada syndrome

Drug induced bradycardia

History

A 73 year old gentleman presents to you following 3 episodes of syncope within one week. He has type 2 diabetes mellitus and glaucoma. His medications include insulin, alfuzosin and he recently commenced timolol eye drops. His wife, who witnessed these episodes, reports that the episodes begin with him complaining of feeling dizzy whilst he was seated, and then losing consciousness. There is no associated seizure activity, tongue biting or incontinence, and blood sugar testing during these episodes does not show hypoglycaemia.

Examination

Cardiovascular and neurological examination is normal with no postural drop between lying and standing blood pressures.

Which investigations should be performed in primary care?

An ECG is key to identify any possible arrhythmia responsible for his symptoms. This shows sinus rhythm at a rate of 54 bpm and is otherwise normal.

What would you do next?

This patient has a clear history of recurrent syncopal episodes and requires further investigation. The next most useful investigation would be a 48-hour Holter monitor and dependent on local services may be directly accessed in primary care or require referral to cardiology. You should advise him that he must not drive and must notify the DVLA.

Outcome

A 48-hour Holter monitor shows sinus rhythm at a rate of 60 bpm with frequent episodes of sinus bradycardia as low as 43 bpm; during the bradycardic episodes the patient reported dizziness. You diagnose him with symptomatic bradycardia secondary to the use of timolol eye drops. His eye drops are stopped, and an alternative is used after advice from ophthalmology. He has no further episodes of syncope and you can now advise him that he can return to driving after 4 weeks.

Learning points

• Timolol is frequently used as a treatment for glaucoma and although it is administered topically, it can spread systemically with no hepatic first pass effect.
• It can be associated with bradycardia and hypotension in older patients and should be used with caution. 
• A drug may unmask underlying cardiac pathology that can recur or persist in the future after the offending drug has been stopped.
  
• 24 Holter monitoring should be considered in patients who have frequent (ideally daily) episodes.

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Hypertrophic obstructive cardiomyopathy

History

A 45 year old HGV driver presents to you after 2 episodes of syncope without any preceding warning and triggers. He has a past medical history of type 2 diabetes mellitus and is taking metformin.

Examination

Cardiovascular examination reveals a loud systolic murmur.

Which investigations should be performed in primary care?

An ECG should be performed and shows normal sinus rhythm with signs of left ventricular hypertrophy.

What would you do next?

He should be advised to stop driving immediately and notify the DVLA. With this history and examination findings he requires urgent referral to a cardiologist for further investigations.

Outcome

The cardiologist organises an echocardiogram which shows evidence of hypertrophic cardiomyopathy.

He undergoes further testing including Holter monitoring and tilt table testing, both of which are normal. He has an insertable cardiac monitor fitted,  which shows paroxysmal atrioventricular block with a long asystolic pause associated with syncope. He is treated with a pacemaker and subsequently remains asymptomatic.

Learning points

• Syncope can be the presenting symptom of hypertrophic cardiomyopathy, often carrying a poor prognosis, and the complex relationship between haemodynamic, arrhythmic and ischaemic causes can make diagnosing the underlying cause of syncope difficult
• Brief self-terminating ventricular tachyarrhythmias, namely ventricular tachycardia and fibrillation, may also induce syncope in patients with HCM
  
• The presence of a new systolic murmur in a patient with syncope mandates further assessment by a cardiologist
• Screening of first degree relatives is recommended
• GP's need to be aware of the DVLA guidance regarding syncope and driving and need to communicate this communicate this to patients and record the advice given.

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Long QT syndrome

History

A 22 year old lady consults with you after a syncopal episode 2 days previously, whilst walking alone. She did not recall any preceding symptoms of chest pain, breathlessness or palpitations. She has no significant past medical history but did recall one previous syncopal episode 4 years previously, which she attributed to a simple faint and was not investigated further at the time. She reports that her brother has previously experienced syncopal episodes.

Examination

Cardiovascular examination is normal.

Which investigations should be performed in primary care?

An ECG should be performed and in this case shows showed a prolonged QT interval of 600ms.

What would you do next?

The diagnosis is likely to be congenital long QT syndrome (LQTS) and she should be referred immediately to a cardiologist for further management. You should advise her not to drive pending further assessment and advice from her cardiologist.

Learning points

• Patients with Long QT syndrome may present to their GP after syncopal episodes and ECG is key in reaching the diagnosis
• Family history present in this case is very important
• There are many types of LQTS. Classification by a cardiologist may point towards different treatments
• It can present at any stage in life and there may be long periods between symptomatic episodes
• Syncope is caused by ventricular tachycardia (Torsades de Points) or fibrillation
• Management consists of avoiding drugs that prolong the QT interval, treatment with beta blockers, and consideration for an implantable cardioverter/defibrillator (ICD) for high risk patients
• Diagnosis should prompt screening of potentially affected family members.

Read the long QT syndrome section.

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Myocardial Ischaemia case history

History

A 46 year old male requests an urgent appointment with you after experiencing a syncopal episode the same morning. He recalls feeling generally unwell and dizzy whilst driving and on exiting his car he lost consciousness. This episode was unwitnessed and the patient is unsure how long his loss of consciousness lasted. On further questioning he reported intermittent epigastric discomfort over the previous two weeks. He is a smoker, has no other significant medical history and is not taking any medication.

Examination

He appears pale but otherwise the physical examination was normal.

Which investigations should be performed in primary care? 

An ECG performed in the surgery is normal.

What would you do next?

The features in this case raise the possibility of vasovagal syncope. However, the patient reports feeling generally unwell and you refer him to the hospital medical team for further assessment.

Outcome

Further investigations in hospital including blood tests are normal. In view of his recent epigastric discomfort, he undergoes a treadmill test which shows ST depression in the first stage of the Bruce Protocol. Subsequent coronary angiography reveals complete occlusion of his left main coronary artery. He is referred to the cardiothoracic surgeons for coronary artery bypass grafting. At his 3 month follow up outpatient appointment, he has had no further symptoms.

Learning points

• Syncope is a rare but recognised presentation of myocardial ischaemia
• It is important to enquire about the symptoms of myocardial ischaemia during the evaluation of syncope to prompt appropriate further investigations and management. In this case, the epigastric discomfort was probably cardiac in origin.
• Routine exercise testing is not recommended for the evaluation of syncope but should be considered in patients with risk factors for coronary artery disease and exercise induced syncope.

Read the Myocardial ischaemia section

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Pulmonary Embolism

History

You are asked to visit a 76 year old lady in a residential home after the staff witness an episode of syncope that morning. Over the past 24 hours she had reported feeling intermittently dizzy. Staff report she appeared clammy prior to her syncopal episode. She has a past medical history of breast cancer treated with mastectomy and chemotherapy 5 years previously.  3 years ago, she had suffered a DVT and had been treated with 6 months of anticoagulation. She also has hypertension and hyperlipidaemia, and her medications include amlodipine, atorvastatin and Adcal D3.

Examination

Physical examination reveals sinus tachycardia of 108 bpm and blood pressure of 156/96. Cardiovascular and respiratory examination are normal.

What would you do next?

The history and the finding of sinus tachycardia raise the possibility of an acute medical problem and she should be referred to the hospital medical team for further assessment.

Outcome

She undergoes further blood tests in hospital including a d-dimer test which is raised. ECG shows sinus tachycardia at 106 bpm and right bundle branch block with an S₁Q₃T₃ pattern. She has a CTPA which reveals bilateral pulmonary emboli and she is treated successfully with thrombolysis.

Learning Points

• Pulmonary embolism can present with non-specific signs and symptoms including syncope
• PE has been reported as the cause of syncope in 0.8% - 1.3% of patients admitted to hospital
• The presence of syncope in patients with pulmonary embolism is a poor prognostic sign as it suggests massive PE with an associated mortality of approximately 30%.

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Aortic Stenosis

History

You are reviewing a 62 year old lady for a cough and find a new systolic murmur. She takes Ramipril for her blood pressure and is otherwise well. 

Examination

Apart from the murmur, cardiovascular examination is normal and her blood pressure is well controlled at 136/78 mmHg.

What would you do next?

She requires an echocardiogram to investigate her murmur further, which demonstrates severe aortic stenosis. She is reviewed by cardiology and has regular follow up planned.

Outcome

Four months later she consults with you after suffering a syncopal episode with no warning whilst walking. You refer her urgently back to her cardiologist.  She undergoes aortic valve replacement and remains symptom free following surgery. 

Learning Points

• Syncope, breathlessness and angina are all symptoms of severe aortic stenosis and the average survival rate after onset of these symptoms is 3 years
• Recent views of this presentation of aortic stenosis are to consider early surgery to protect the left ventricle
• Syncope, breathlessness or anginal chest pain in patients with known aortic stenosis should prompt urgent referral to a cardiologist for consideration of surgical valve replacement or transcatheter aortic valve implantation (TAVI) to prevent symptoms and improve prognosis and survival.

Read our section on Aortic stenosis

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Atrial Fibrillation

History

A 36 year old nurse presents to you with episodes of dizziness, palpitations and breathlessness lasting several minutes. She has no significant past medical history and does not take any medications She develops syncope during half of these episodes. There are no precipitating factors and the episodes resolve spontaneously. When she develops syncope, she recovers rapidly.

Examination

Cardiovascular examination and postural blood pressures are normal.

What would you do next?

You should advise her not to drive and notify the DVLA. She should have an ECG (which is normal), blood tests including thyroid function testing and be referred to a cardiologist to investigate her palpitations and syncope further.

Outcome

Whilst awaiting her cardiology appointment she continues to have episodes and on one occasion attends A&E where her ECG reveals normal sinus rhythm again. The A&E team organise a Holter monitor for 24 hours and there are no reported episodes during this period and no abnormal ECG changes. 

She consults with a medical colleague who considers a diagnosis of anxiety with panic attacks, and she engages with psychological therapy to manage anxiety but continues to experience symptoms.

She is reviewed by a cardiologist and an insertable cardiac monitor (ICM) is implanted. 3 months later she has another episode and the ICM demonstrates atrial fibrillation with a rapid ventricular response. She undergoes successful ablation therapy, and has no further episodes.

Learning Points

• Paroxysmal Atrial Fibrillation is a relatively uncommon cause of syncope.
• Short term monitoring of infrequent episodes of pre syncope or syncope (e.g 24 hour ECG/Holter monitor) has a low yield.
• Implantable devices, although more expensive, should be considered with infrequent episodes to improve the diagnostic yield and may be cost effective.

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Brugada Syndrome

History

A 24 year old man of South-East Asian origin, presents to you after experiencing 3 episodes of syncope over two 2 months. He reports loss of consciousness for a few seconds before rapid recovery. These episodes are not associated with precipitating factors and there are no other associated symptoms. He has no significant personal past medical history. However, his father died unexpectedly age 32 in a drowning accident whilst snorkelling on holiday.  

Examination

Cardiovascular examination and postural blood pressures are normal.

What would you do next?

You should advise him not to drive and notify the DVLA. He should have an ECG, which shows sinus rhythm and atypical right bundle branch block, and you refer him urgently to a cardiologist for further assessment.

Outcome

His cardiologist recognises the ECG pattern as type 1 Brugada Syndrome. An echocardiogram is normal. An implantable cardioverter defibrillator is inserted, and no further episodes of syncope occur. His family are screened for Brugada Syndrome.

Learning Points

• Brugada syndrome, a genetically determined channelopathy, can cause syncopal episodes or sudden death due to ventricular tachyarrhythmias in patients with a structurally normal heart
• ECGs can show changes that resemble right bundle branch block with coved ST elevation in leads V1 - V3 (Type 1 Brugada)
• In some patients with Brugada Syndrome the ECG can be normal and for diagnostic purposes, abnormalities can be induced in the laboratory by infusion of anti-arrhythmic agents
• As Brugada Syndrome is inherited, enquiries should be made regarding family history. First degree relatives should be screened
• There is no effective drug therapy for Brugada Syndrome and implantable cardioverter defibrillators (ICDs) are indicated in some patients to prevent sudden death
• Unexplained drowning may be a manifestation of sudden cardiac death.

Brugada syndrome section of the toolkit

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Other types of blackout and syncope

In this section: 

• Syncope of unknown origin
• Epilepsy and syncope
• ‘Psychogenic’ pseudo-syncope (PPS)
• Rare causes of blackouts
• Non-haemodynamic collapse / Psychogenic Pseudosyncope (PPS) case history
  

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Syncope of unknown origin

Reported diagnostic rates can vary considerably depending on a number of factors including the setting in which patients were reviewed, the special interests of the clinicians, whether syncope guidelines are followed, and whether patient who fainted sought medical advice.

In a 2002 study reviewing patients in the original Framingham Heart and Offspring studies, a cause for syncope was not identified in 36.6% of patients, although this study included patients who reported fainting but did not seek medical help and were therefore categorised as ‘undiagnosed’.

In another study where European Society of Cardiology Syncope Guidelines were very carefully followed, 2% of patients remained undiagnosed after investigations. In recent analysis of 10 Syncope Units, a no-diagnosis-rate of the order of 10% was reported.

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Epilepsy and syncope

In comparison with syncope, epilepsy is much rarer, affecting a little under 1% of the UK population.

• Ictal or epileptic asystole – bradycardia and asystole are rare occurrences during partial complex seizures
• Syncopal epileptic seizures – brain hypoxia as a consequence of syncope can trigger epileptic seizures.

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‘Psychogenic’ pseudo-syncope (PPS)

There are two main types of conversion disorder associated with blackouts:

• Non-epileptic Seizures (NES) – where limb movements are marked. These can be diagnosed using video or EEG monitoring.
• ‘Psychogenic’ Pseudosyncope (PPS) – episodes which resemble syncope and limb movements are minimal. PPS is collapse which is associated with maintained blood pressure and slightly increased heart rate without the impairment of cerebral circulation that occurs in vasovagal syncope (VVS).

Terminology

There is controversy around the terminology used to describe these episodes. Collapses that look like other conditions but are not explained by the same physiological mechanisms have tended to fall under as many labels as there are specialties encountering them. Hence historically within neurology the term ‘non-epileptic seizures’ is favoured, within cardiology ‘psychogenic pseudosyncope’, and within psychiatry ‘conversion disorders’.

The authors favour the terms non-haemodynamic and non-epileptic collapse; we hope this will be considered and recommended in future working groups but recognise that this is not yet accepted practise. Having taken advice on this with our steering committee and especially patient representatives, it was agreed that an accepted label that enables referral to the appropriate treating specialty is the priority meantime, and hence ‘psychogenic’ pseudosyncope (PPS) is used within this document.

Diagnosis

PPS is not just a diagnosis of exclusion, but in fact such episodes can be diagnosed by appropriate history taking, with very frequent episodes being the main feature.

Diagnosis can be made when episodes are monitored by simultaneous video, beat-to-beat blood pressure and ECG recordings on a tilt-table, without hypotension/bradycardia and confirmed by the patient as being a typical attack. Importantly, there is increasing evidence that both VVS and PPS can commonly both occur in the same patient. Thus, the presence of one does not exclude the other, but different treatment approaches may be required for each.

It is important to be clear that these collapses are outside of the patient’s conscious control and are therefore not malingering or attention seeking behaviours.

Management

Timely delivered psychological therapies to provide reassurance and improve functionality are the primary treatment modalities.

Psychotropic medications may need to be considered in patients with comorbid psychiatric disorders. There is limited evidence for therapy efficacy in PPS, however studies in related conversion disorder populations supports use of psychotherapy. Appropriate interventions include improving detection of bodily sensations and stress markers, and especially in PPS the treatment of underlying anxiety, stress or trauma. Working with a practitioner experienced in this area, motivated patients, with sufficient cognitive capacity for self-insight, can be optimistic of becoming PPS episode free.

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Rare causes of blackouts

Vertebro-basilar TIA – rarely causes syncope and always associated with neurological signs including nystagmus, dysarthria, limb weakness, ataxia, vertigo and diplopia.

Subclavian Steal – this is a rare phenomenon which occurs if blood flow is reversed in the vertebral artery toward the ipsilateral distal subclavian artery by the demand for flow to the exercising arm of the same side. The cause is a narrowing or occlusion of the proximal subclavian artery. The phenomenon is associated with neurological signs.

G-induced loss of consciousness (G-LOC) – this is due to the centrifugal effect of rapid acceleration. Although rare, it is common in aircrew, and was experienced by 15% of RAF crew in 2015, mostly during training. G-LOC has been associated with air crash fatalities.

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Case history: Non-haemodynamic collapse / Psychogenic Pseudosyncope (PPS)

History

A 19 year old boy attends with his mother with a history of multiple syncopal episodes in the previous 24 months.  They report frequent and witnessed episodes of syncope with several episodes occurring in a single day. There are no associated triggers or warnings of the attacks. He has no significant past medical history but also reports symptoms of body aches, fatigue and generalised weakness. You note that he has already undergone extensive investigations under a paediatrician 2 years ago including ECG, echocardiogram, Holter monitoring and EEG which were all normal. He and his family were frustrated that no cause was previously found for his symptoms and did not attend follow up after his tests.

Examination

Physical examination is normal and postural blood pressures show no significant drop.

What would you do next?

There are no further investigations in primary care that would provide additional useful information. He requires further assessment from a dedicated syncope service.

Outcome

The syncope service organise tilt table testing and after 6 minutes of tilt he develops a sudden loss of consciousness with no response to verbal stimuli. Monitoring demonstrates no significant changes in heart rate, blood pressure, and no ECG changes. He is diagnosed with psychogenic pseudo-syncope (PPS) and was referred to a psychologist after full explanation to him and his family of what had happened.

Learning Points

• Tilt table testing can induce psychogenic syncope i.e apparent loss of consciousness without a change in recorded blood pressure and EEG. A slight tachycardia if 10-20 bpm is to be expected
• Diagnosis is based on the history and can be confirmed when a typical event is recorded during a tilt-table test with simultaneous BP, HR, EEG and video recordings of the patient
• Some factors can help distinguish PPS from vasovagal syncope
• Eyes are usually closed in psychogenic syncope but open in VVS
• Recurring multiple collapses in a single day suggest PPS.

Differentiating vasovagal syncope epilepsy and psychogenic pseudosyncope

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Initial assessment of the syncope patient

In this section:

• History taking
• Examination
• Red flags in syncope
• Risk stratification tools.

History taking

Things to ask the patient (and preferably a witness)

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Examination of patient

• Cardiovascular examination
• Neurological examination if indicated by the history
• Other systems as appropriate
• Active stand test.

Within a 10-minute consultation, it may be impossible to conduct all aspects of the assessment and it may be necessary, after risk assessment, to arrange a follow-up consultation.

Risk stratification tools

Risk stratification tools are of limited value and have not been shown to perform better than good clinical judgement in identifying patients at high risk of serious short-term outcomes. Most risk assessment tools were developed for use in the emergency department and no risk assessment tools have been validated in primary care.

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Syncope educational resources for healthcare professionals

• Transient loss of consciousness ('blackouts') in over 16s - clinical guideline [CG109], last updated: 01 September 2014
• European Society of Cardiology - Guidelines on diagnosis and management of Syncope, 2018
• 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of Postural tachycardia syndrome, Inappropriate sinus tachycardia, and Vasovagal syncope
• Syncopedia is a website containing free, high quality syncope education. It is targeted at students, residents, nurse specialists and physicians that want to learn more about syncope.

Primary care syncope checklist

The syncope checklist for GPs helps to identify red flag symptoms and signs that require urgent hospital referral or cardiology opinion, and also features that point towards vasovagal syncope and orthostatic hypotension.

Download the syncope checklist for GPs (847 KB PDF)

Differentiating vasovagal syncope epilepsy and psychogenic pseudosyncope

Adapted from the 2018 ESC Guidelines for the diagnosis and management of syncope and IF IT'S NOT EPILEPSY PEM Smith 2001.

The inducing syncope video shows induced vasovagal syncope and demonstrates the convulsive movements on vasovagal syncope that may lead to a misdiagnosis of epilepsy.

Management of syncope

See the section on Cardiac syncope for management of individual cardiac conditions.

In this section:

• Self-care measures
• Physical counterpressure manoeuvres
• Medication
• Pacemakers
• Psychological support
• Driving advice.

Self-care measures

The following are useful techniques to relieve symptoms and prevent syncope in the following conditions:

• Vasovagal syncope (VVS)
• Orthostatic hypotension (OH) - useful in many types of OH (but not in acute volume depletion)
• Postural tachycardia syndrome (PoTS).

Self-care measures include:

• Reduce or remove culprit medications
• Avoiding triggers such as prolonged standing, heat, alcohol
• Maintaining good fluid intake of 2-2.5 litres a day in adults - advise two cups of water before rising
• Additional salt, from 6-10g a day (unless contraindicated)
• Diet, for example regular meals, fibre to prevent straining in defaecation syncope and avoid heavy meals in post-prandial hypotension
• Compression such as waist high tights or compression sports clothing, abdominal binder
• Maintaining fitness
• Postural counterpressure-manoeuvres (see images below)
• Medical alert bracelets can be useful for people who faint regularly.

Physical counterpressure manoeuvres

These measures can raise blood pressure in VVS and OH, and lower heart rate in PoTS.

Images used with consent of Prof Wouter Wieling.

This short YouTube video 'How can I prevent a syncopal episode?' describes how patients with vasovagal syncope can prevent syncope using postural countermeasures.

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Medication

See the section on Cardiac syncope for medication in cardiac conditions.

Medication used in orthostatic hypotension, vasovagal syncope and PoTS:

• Medication should be used if self-management techniques have failed to improve symptoms and is used in combination with these
• The evidence base for medication is limited
• Drugs mostly aim to increase blood volume and constrict blood vessels. In PoTS some also aim to blunt the tachycardia
• The only medication listed below that has marketing authorisation (‘is licensed’) for the use indicated is midodrine for refractory orthostatic hypotension. Others may be prescribed under a shared care agreement.

Medication used in V V Syncope, OH and PoTS

Download Medication used in V V Syncope, OH and PoTS (52 KB PDF)

Evidence for medication in VVS, OH and PoTS

+ may be used in this condition, weaker evidence

++ stronger evidence for use of this medication

Pacemakers

In vasovagal syncope with asystole, cardiac pacing may be effective in preventing syncope when tilt testing is negative. Pacing shows less benefit in tilt positive patients, possibly because the latter may faint primarily due to the vasodepressor response (blood pooling) which will not respond to pacing. The former may have more dominance of cardio-inhibition (vagal) response.

Pacemakers should be avoided if possible in people under the age of 40.

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Psychological support

Syncope and quality of life

There are significant quality of life implications for people experiencing syncope.

"The experience of VVS is at best inconvenient, and may be [self]-perceived as threatening and disabling.” (Gracie, Baker, Freeston and  Newton 2014)

Quality of life impact has been equated to severe rheumatoid arthritis or chronic low back pain. Fear of an episode can result in a pattern of avoidance behaviours, which can increase the likelihood of further anxiety-precipitated neuro-cardiogenic or non-haemodynamic syncopal events. This can lead to a vicious cycle of increased fear, avoidance and despondency.

Associated isolation and impacts on activity levels can lead to depression, which has been demonstrated to have implications for adherence to health-related behaviours in other health conditions including cardiovascular disease.

Psychological assessment and therapeutic intervention

Psychiatric or psychological assessment may be considered for all patients experiencing syncope. As well as adjustment-related distress, it has been suggested that psychological issues can be associated with the development and maintenance of VVS. Rates of anxiety and depression are higher in people experiencing VVS than for matched healthy controls, and worsen with the increasing frequency of episodes and certainly treatment of any co-morbid psychiatric disorders using current treatment guidelines will be critical to optimise outcome.

Pharmacological treatment

There has been some evidence of serotonin’s role in blood pressure regulation in VVS, and some evidence that SSRIs can be beneficial, but trial data is unconvincing. However, it is unclear whether this is due to a direct effect on the physiological mechanism, the effect of an improvement in mood, or the interaction of these.

Psychotherapy

Currently the efficacy of CBT for syncope has been demonstrated in a series of case-studies (Newton, 2003) leading to a decrease in episodes and subjective improvement in quality of life and return to work or school.

This study focused on identifying and restricting unhelpful beliefs, addressing maladaptive somatic attention, reducing avoidance, improving a sense of control over symptoms with applied tension for example, as well as the individual’s more idiosyncratic challenges such as sleep, relationship struggles associated with compromised health and avoidance, and hopelessness about the future.

Other important factors include treating underlying disorders, reducing guilt, shame and frustration associated with ill-health, and helping patients focus on how to still live a rewarding and fulfilling life even with their physical limitations.

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Driving advice

Assess all syncope patients for fitness to drive. As driving advice is changed regularly, always check the DVLA website (or equivalent organisation if outside the UK) for up to date guidance. At the time of writing in 2020:

• Group 1 drivers - in general, patients with uncomplicated vasovagal syncope that only occurs when standing may drive and need not notify the DVLA
• Group 2 drivers – all group 2 drivers with syncope of any cause should cease driving immediately and must notify the DVLA
• There are many more complicated scenarios including syncope whilst seated, cough syncope, cardiac syncope, and unexplained syncope where guidance is complex and variable, and the guidelines should be consulted for detailed advice.

*Record the advice that you have provided regarding driving in the patient’s medical records.

Visit GOV.UK for up to date advice about driving in the UK.

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Investigations

In this section:

• Electrocardiogram (ECG)
• Blood tests
• Active stand test
• 24-hour ambulatory and home blood pressure monitoring (ABPM, HBPM)
• Holter monitor
• Implantable cardiac monitor (ICM) previously known as insertable loop recorder (ILR)
• Tilt table test
• Autonomic tests
• Exercise testing
• Tests of low clinical value
• Syncope of unknown origin case history.

Electrocardiogram (ECG)

All patients with an unexplained blackout should have a 12 lead ECG with automated interpretation. If this is unavailable, a manual ECG should be recorded and analysed by a healthcare professional who is trained and competent at reading ECGs.

ECGs patterns in children and adolescents can vary with age and are different from those of adults.

Reasons to use ECGs:

• European Society of Cardiology guidelines for the diagnosis and management of syncope recommend ECG as the first investigation for syncope
• A comprehensive history, examination (including postural blood pressure measurements) and ECG can diagnose a cause of syncope in 23-50% of patients
• ECGs are a non-invasive, inexpensive tool for identifying a cause and helping guide prognosis and risk stratification.

What an ECG can tell you in syncope:

• ECGs are more likely to identify ischaemic, structural or conduction abnormalities than arrhythmias, many of which are paroxysmal
• Abnormal ECG findings occur in 90% of patients with cardiac-induced syncope but in only 6% of patients with vasovagal syncope
• A normal ECG makes it unlikely that an arrhythmia is the cause of syncope, and these persons are at low risk of sudden death
• A normal ECG can be helpful in reducing the need for further investigations including echocardiography.

ECG red flags in syncope 

The following are examples of ECGs that are red flags in syncope and should prompt consideration of urgent assessment of the patient presenting with syncope.

• Sinus bradycardia
• Sinus pauses/prolonged asystole
• AV block – 2nd degree (types 1, 2) and complete heart block
• Bundle branch blocks - right and left bundle branch block and 'trifasicular' block
• Atrial fibrillation and atrial flutter
• Wolf-Parkinson-White syndrome
• SVT
• Ventricular tachycardia, Torsades de Pointes and ventricular fibrillation
• Long QT
• Short QT
• Brugada syndrome
• ARVC
• Ischaemic heart disease ef anterior myocardial infarction, old inferior myocardial infarction
• ST-T wave changes
• Left ventricular hypertrophy (LVH) or right ventricular hypertrophy
• Pulmonary embolism
• Pacemaker malfunction.

We would like to thank Dr Dean Jenkins, Stephen Gerred and Prof Richard Sutton for providing these images. Further ECG images can be found on ECG Library.

Blood tests

Consider the following points about blood tests:

• Routine blood tests are rarely cost effective in adults with syncope unless guided by clues in the history suggesting an underlying diagnosis, for example diabetes or gastrointestinal (GI) blood loss
• It can be helpful to check for iron deficiency in children
• May be helpful in detecting metabolic abnormalities such as electrolyte abnormalities to explain loss of consciousness if witness account not available
• Some studies have proposed a role for using B-type natriuretic peptide (BNP) or high sensitivity Troponin I, which add evidence of the existence of structural heart disease for predicting adverse outcomes in syncope, but it is too early to recommend for routine clinical practice.

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Active stand test

The active stand test is sometimes called ‘the poor man’s tilt table test’ by patients. It is useful in identification of orthostatic hypotension (classic and immediate types), and PoTS (when it may also be called 'the 10 minute NASA learn test').

How the active stand test works:

• The patient is rested supine, then asked to stand up (ideally against a wall or in front of a chair to minimise injury if the patient starts to feel faint)
• A manual or battery-operated sphygmomanometer can be used to repeatedly record heart rate and blood pressure whilst supine then for a minimum of 3 and up to 10 minutes while standing.

Continuous beat-to-beat non-invasive blood pressure and heart rate monitoring in a laboratory in secondary care will yield more detailed information than a manual blood pressure monitor and may be performed in conjunction with a tilt test. Active stand employs the leg muscle pumps while tilt testing does not and therefore they reveal different haemodynamic effects.

24-hour ambulatory and home blood pressure monitoring (ABPM, HBPM)

Points to consider with ABPM and HBPM:

• May be useful to investigate unexplained syncope especially in older patients with one study showing 25% of elderly patients admitted with falls or syncope had post-prandial hypotension especially after breakfast.
• ABPM is recommended to detect a degree of orthostatic hypotension, supine hypertension and nocturnal hypertension in patients with autonomic failure.
• ABPM and HBPM may be considered to detect whether blood pressure is abnormally low during episodes suggestive of orthostatic intolerance. A symptom diary during monitoring can be helpful.
• ABPM may be more useful than tilt table testing to evaluate orthostatic hypotension.
• ABPM can evaluate BP over a longer time period than tilt table testing, counteract the effect of white coat hypertension and provide insight into blood pressure variations during the day which may be influenced by food, posture and medication. ABPM can also be useful to detect overtreatment of hypertension which can result in syncope, but its limitation is the relative infrequency of BP measurements.

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Holter monitor

Holter monitors are of limited value and only useful if syncope or presyncope symptoms are very frequent, for example daily. Other points to note:

• Holter monitors allow continuous ECG monitoring from 24-48 hours to 1-2 weeks.
• 24-hour Holter monitoring is of limited benefit due to the short duration of monitoring and ECG rhythm and symptom correlation is rarely achieved. 24-hour Holter monitoring should be considered in patients who have frequent (ideally daily) episodes.
• Diagnostic yield  is reported to be as low as 1-2% in unselected patients.
• They have a greater sensitivity in achieving diagnosis in those with cardiac syncope but the frequency of events must be high and this suggests a need for in-hospital monitoring.
• Normal Holter monitoring does not exclude arrhythmia as a cause of syncope if no event occurs.
• Holter monitoring may show evidence of arrhythmias in normal, asymptomatic individuals.
• Extending monitoring to 72 hours increases the number of asymptomatic arrhythmias detected but not overall diagnostic yield.
• Prolonged external loop recording, for example 14 days, has a higher diagnostic yield than conventional Holter monitoring, forming an interim strategy between Holter and implantable cardiac monitor.   

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Implantable cardiac monitor (ICM) previously known as insertable loop recorder (ILR)

Image courtesy of Dr Alexander Breitenstein, Journal of Cardiovascular Medicine.

The ICM is a small device which is implanted subcutaneously within the chest wall and monitors heart rate continuously. They are designed to record abnormal heart rhythms and can remain under the skin for up to four years.

Indications

• In suspected reflex syncope, where the diagnosis is not clear after initial evaluation
• In patients with suspected cardiac cause of syncope, consider if syncope is less frequent than every 1-2 weeks
• Suspected epilepsy where arrythmia should be excluded
• Unexplained falls
• Inherited arrhythmia disorders or primary cardiomyopathy where there is low risk of cardiac death (alternative to ICD)
• ICMs are valuable in detecting infrequent arrhythmias and can be programmed for automatic and patient activated detection.

Insertion

ICMs can be inserted just underneath the skin over the chest wall, usually close to the left sternal edge, via a minimally invasive procedure. They have no external parts and can transmit data to a diagnostic station via automatic or simple patient demand. Implantation is associated with a low rate of infection (1-4%). Although currently they are mostly inserted in a hospital setting, they have occasionally been implanted by GPs in their surgery.

Advantages of ICM

The advantages of ICM include:

• Long term ECG monitoring with an ICM extends the monitoring period up to four years compared with the very short period of Holter monitoring, reduces patient non-compliance and does not prohibit physical activity
• Early use of ICM enables treatment, including pacing, to be delivered more safely, specifically and effectively
• Use of ICMs reduces the number of A&E attendance in patients with recurrent syncope.

Diagnostic yield

ICMs have been found to be more cost effective than conventional strategies and are more likely to provide a diagnosis in patients with recurrent unexplained syncope.

The estimated diagnostic yield of the following investigations used in syncope is:

• 1–5% for a 24–48 hour standard Holter monitor
• 5–10% for a 3–7 day external ECG or event recorder
• 15–25% for a 1–4 week external ECG or event recorder
• 30–50% for a ≤ 36 month ICM
• 80% for 48 months.

ICMs have higher diagnostic rates in older patients and can provide a diagnosis in 20% of patients aged over 50 with unexplained recurrent falls and normal initial cardiac evaluation.

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Tilt table test

Image courtesy of Syncope Unit at Hammersmith Hospital, Imperial College Healthcare NHS Trust.

Procedure

The tilt table test is performed in a room where resuscitation equipment is rapidly available. The patient lies supine on a tilting bed with a footplate and straps. The test starts with the patient resting still in a supine position for between five and over 20 minutes, and then is tilted head up to 60-70 degrees for approximately 20-45 minutes.

If there is no response, sublingual GTN spray or an isoproterenol infusion may be administered. Carotid sinus massage may be performed in patients over 40 years of age. The patient is monitored throughout and either syncope is induced, or the test protocol is completed.

Points to consider with the tilt table test:

• Tilt table testing is a more useful investigation than Holter monitoring in diagnosing suspected vasovagal syncope
• The test is time consuming and requires experienced staff and technical equipment, varies in its reproducibility and does not reproduce completely a spontaneous syncope
• Head-up tilt table testing is safe with very few reported adverse events.

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Autonomic tests

Laboratory testing of the autonomic nervous system can help when autonomic dysfunction is the possible cause of syncope.

• The most widely used test of cardiac parasympathetic function is heart rate variability
• Heart rate responses to a Valsalva manoeuvre examine sympathetic function
• Common tests of sympathetic adrenergic function include the blood pressure response to postural change with tilt table testing and active standing
• Autonomic function testing provides a safe, effective way to further evaluate patients presenting with syncope and can be diagnostic for autonomic failure (for example pure autonomic failure, multisystem atrophy, Parkinson’s disease), classical and delayed orthostatic hypotension, vasovagal syncope, and PoTS.

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Exercise testing

Exercise stress testing is indicated in patients whose syncope is related to exercise. The test involves the patient undertaking exercise (usually on a treadmill) whilst attached to an ECG monitor.

When syncope occurs during exercise, urgent exercise testing should be considered. Advise the patient to avoid exercise until seen by their secondary care specialist. Exercise testing is usually contraindicated in aortic stenosis and hypertrophic cardiomyopathy (these conditions can cause syncope on exercise).

• Unselective exercise testing delivers a poor diagnostic yield in the investigation of syncope
• Investigation with exercise stress testing can lead to the diagnosis of ischaemia or arrhythmias precipitated by exercise, in contrast to post-exertional vasovagal syncope that may be associated with autonomic dysfunction.   

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Tests of low clinical value

The following tests are of low diagnostic yield in syncope and should not routinely be offered unless specifically indicated:

Tilt test – should not be offered to the patient with clear history of vasovagal syncope unless there is a strong need for confirming the diagnosis or for further patient education (see above).

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Case histories

• Syncope of unknown origin case history

Case history: Syncope of unknown origin

History

A 59 year old man consults with you describing a history of recurrent syncope. He reports seven episodes of syncope in the previous 12 months with rapid onset, no warning signs and no apparent triggers. He has no significant past medical history and takes no medications.

Examination

Cardiovascular examination is normal.

What would you do next?

You should advise him that he must not drive, and he must notify the DVLA. He requires further evaluation with an ECG (which is normal). He should also be referred to a cardiologist.

Outcome

His cardiologist organises further tests including carotid sinus massage, tilt table testing and echocardiogram which are all normal. He receives an insertable cardiac monitor (ICM), and 9 months later experiences a syncopal episode associated with a recorded 21 second asystolic pause. His diagnosis is asystolic vasovagal syncope. Lifestyle changes do not improve his symptoms as he has no warning an no clear triggers. He subsequently has a pacemaker fitted with no further episodes of syncope.

Learning Points

In cases of recurrent syncope with no evidence of structural heart disease on initial assessment and normal ECG, ICMs can provide evidence of the underlying cause.

• Syncope in children and young adults
• Pregnancy and syncope
• Syncope in athletes
• Falls and syncope

Syncope in children and young adults

In early childhood:

• Vasovagal syncope in young children or Reflex Anoxic Seizures (RAS) - see more on vasovagal syncope in younger children.
• Cyanotic (or blue) breath holding spells or reflex expiratory apnoea syncope or infantile reflex expiratory apnoea syncope – this is a common phenomenon and tends to occur when children stop crying after prolonged crying

In late childhood and young adults:

• Vasovagal Syncope – there is a peak incidence of VVS around the age of 15, and it is twice as common in females compared to males
• Initial orthostatic hypotension
• Postural tachycardia syndrome – not all people with PoTS experience syncope
• Mess trick or the ‘Fainting Lark’– the person first hyperventilates while squatting, then standing up quickly, strains (valsalva manouevre) then faints
• Adolescent stretch syncope – a rare phenomenon seen in teenagers and young adults. It is due to hyperextension of the neck and mechanical compression of the vertebral arteries.

See sections on Cardiac syncope and Syncope and sudden death in athletes.

Further reading

• SADS (Sudden Arrhythmia Death Syndrome) Foundation - Provides support and information for patients and families affected by SADS and aims to raise public awareness.
• CRY - Cardiac Risk in the Young - Works with cardiologists and GPs to promote and protect the cardiac health of young people by establishing good practice and facilities to reduce the frequency of young sudden cardiac death.

Read Anomalous origin of left coronary artery in a child with syncope case history

Case histories

• Anomalous origin of left coronary artery in a child with syncope

Case history - Child with syncope

History

A normally fit and well 12 year boy, with no significant past medical history developed shortness of breath during sports lessons at school. There was no significant medical history, he took no medication and there was no family history of cardiac disease or sudden death.

Examination

An ECG, FBC and U+E were normal

What would you do next?

You would refer him to a paediatrician to further evaluate his symptoms,

What happened next?

He was referred to a paediatrician with an interest in cardiology. He was investigated with an exercise treadmill test, which was normal.

2 years later, age 14, he developed syncope during a football match. An emergency ambulance was called and assessment by the paramedics revealed he was in ventricular fibrillation. He was successfully resuscitated with cardioversion and transferred to hospital for further assessment. ECG showed normal sinus rhythm with no ischaemic changes.

He went on to have an echocardiogram which revealed anomalous origin of the left anterior descending artery. This was confirmed on coronary angiography and repaired surgically.

Learning Points

• Anomalous origin of a coronary artery due to obstruction in its path or flow abnormalities, is associated with an increased risk of myocardial ischaemic during exercise and subsequent ventricular arrhythmias. It is the third most frequent cardiac cause of deaths associated with exercise among athletes aged 12-35 years
• Almost 50% of patients report symptoms including syncope, chest pain, and breathlessness prior to sudden death
• Coronary abnormalities are amongst the most common congenital cardiovascular anomalies, surpassing in prevalence nearly all others combined. Many congenital coronary abnormalities have a benign outcome
• Anomalous origin of the left coronary artery cannot be excluded by normal ECG and normal exercise treadmill tests
• Echocardiography is a key investigation when assessing young patients with syncope or chest pain associated with exercise.

Pregnancy and syncope

Syncope occurs in up to 4.6% of pregnancies. Most women with vasovagal syncope (VVS), orthostatic hypotension (OH) and postural tachycardia syndrome (PoTS) will have a safe delivery and a healthy baby. However, syncope may be associated with slightly higher rates of adverse outcomes including preterm births and congenital anomalies, and an increased incidence of maternal cardiac arrhythmias and syncope in the first-year postpartum.

In this section: 

• Causes of syncope in pregnancy
• Risks of VVS, OH and PoTS in pregnancy
• Supine hypotensive syndrome
• Palpitation and arrhythmias in pregnancy
• Planning a pregnancy with syncope
• Safety in pregnancy of medication used in VVS, OH and PoTS
• Self-care measures for VVS, OH and PoTS in pregnancy
• Labour and delivery
• Anaesthetic considerations
• Postnatal period
• Syncope investigations in pregnancy
• Devices in pregnancy.

Causes of syncope in pregnancy

Causes of syncope and low blood pressure in pregnancy include:

• Vasovagal syncope
• Pulmonary embolism
• Haemorrhage eg ruptured ectopic pregnancy, aortic dissection
• Uterine rupture
• Amniotic fluid embolism
• Cardiac causes include peripartum cardiomyopathy, coronary or aortic dissection, SVT, VT
• Supine hypotensive syndrome (aorto-caval compression)
• Orthostatic hypotension
• In relation to PoTS.

Non syncopal causes of blackouts in pregnancy:

• Hypoglycaemia
• Eclamptic seizures.

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Risks of VVS, OH and PoTS in pregnancy

Vasovagal Syncope - occasional report of abruption, fetal hypoxia.

Low blood pressure – some small studies suggest a slight reduction in birth weight and increase in stillbirth. Mechanism and management is unclear.

PoTS – pregnancy is safe in PoTS for mum and baby. No increase in miscarriage, preterm delivery, stillbirth or perinatal mortality.

Paternal syncope is not uncommon and is also a risk! Trauma to both mother and father can occur.   

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Supine hypotensive syndrome

Points to consider:

• This occurs due to aorto-caval compression
• Within 3-7 minutes, around 30% of the effective circulating blood volume can be effectively lost and significant hypotension occurs
• Can occur from 19 weeks of pregnancy – when supine
• Effect on mum: hypotension associated with dizziness, pallor, sweating, nausea, syncope or near syncope, tachycardia (bradycardia in late stages), lower limb oedema
• Effect on baby: fetal hypoxia or death
• Management – turn onto left side when supine or sit upright.

Palpitation and Arrhythmias in pregnancy

The majority of arrhythmias in pregnancy are not harmful. However physiological changes in pregnancy may trigger arrhythmias, some of which can lead to syncope.

Benign palpitations – it is normal for heart rate to increase by 25% in pregnancy, and ectopic beats occur in around 50%, and both therefore cause palpitations.

Structural heart disease - this may present for the first time in pregnancy, for example mitral stenosis. In women with known structural heart disease (such as congenital heart disease, acquired valvular disease, cardiomyopathy), arrhythmia is a predictor of a cardiac event during the pregnancy and should therefore be treated as a red flag. Women with structural heart disease may require referral to a tertiary obstetric centre to plan a safe pregnancy and delivery.

Electrical heart disease – such as accessory pathways or Wolff-Parkinson-White, AV-nodal re-entrant tachycardia, channelopathies, drug-related long QT.

Planning a pregnancy with syncope

When planning a pregnancy with syncope, you should:

• Provide the usual preconception advice
• Maximize wellness before pregnancy – self-care measures
• Stop any drugs that are contraindicated - see UKTIS website
• Counsel the patient regarding the risk and benefit of continuing drugs and seek secondary care consultant advice where appropriate
• Consider any associated conditions which may impact the pregnancy such as cardiac disease, hypermobile Ehlers-Danlos syndrome, chronic fatigue syndrome and autoimmune conditions
• Refer to specialist maternity services if syncope is due to a cardiac cause for preconception advice - find out more about cardiac disease and pregnancy from the Royal College of Obstetricians and Gynaecologists.

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Safety in pregnancy of medication used in VVS, OH and PoTS

Table adapted from consensus document 2007.

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Self-care measures for VVS, OH and PoTS in pregnancy

Self-care measures include:

• High fluid intake (unless contraindicated)
• Increase salt (unless contraindicated)
• Compression tights or stockings
• Some women will improve as pregnancy progresses; this is thought to be related to the 50% increase in plasma volume in late pregnancy.

Labour and delivery

In general the management of the delivery follows normal obstetric guidelines and is not altered by the fact that the patient experiences syncope.

Note that:

• Upright posture and warm baths should be avoided
• Squatting may relieve symptoms, but standing up after squatting may exacerbate them.

Anaesthetic considerations

Anaesthetic considerations include:

• Hypotensive tendency or intraoperative hypotension
• Epidurals and spinals can be used but can worsen hypotension
• Early use of intravenous infusion, especially if fasting.

Postnatal period

Things to consider in the postnatal period: 

• Early mobilisation after delivery
• Extra fluids when breast feeding
• Consider compression tights
• Pacing of activities.

In PoTS, most women report improvement 6-12 months after pregnancy

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Syncope investigations in pregnancy

Considerations for syncope investigations in pregnancy:

• Mostly investigations can wait unless cardiac syncope is suspected
• Echo, exercise ECG and some pharmacological challenges may be undertaken
• Active stand test can be undertaken in pregnancy
• Tilt test is contraindicated in pregnancy
• Symptom diary and heart rate or blood pressure recordings can be helpful.

Devices in pregnancy

Considerations for devices in pregnancy:

• Insertable Cardiac Monitors (ICMs) are not contraindicated in pregnancy
• DC cardioversion can be safely administered where necessary throughout pregnancy
• pacemakers – should be avoided if possible under 40 years old - however, insertion of a pacemaker during pregnancy does not appear to cause maternal or fetal complications
• women with implantable cardioverter defibrillators (ICDs) have achieved successful pregnancies, even when the devices have been triggered.

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Syncope in athletes

The European Heart Rhythm Association (EHRA) estimates that one to two per 100,00 athletes under 35 years old die suddenly each year, with higher rates in males and Afro-Caribbean people.

In this section:

• Syncope and sudden cardiac death (SCD) in athletes
• Exercise-related syncope
• Screening
• The role of the GP in preventing sudden cardiac death in athletes.

Syncope and sudden cardiac death (SCD) in athletes

Key facts:

• A retrospective study found that 29% of athletes who died suddenly during competition had previously had symptoms suggesting cardiac disease
• Most individuals that suffer SCD are asymptomatic, but syncope has been reported as the most common symptom before SCD
• Pre-syncope carries the same prognostic implications as syncope
• Syncope may be the presenting symptom of several conditions (hypertrophic cardiomyopathy, ARVC, anomalous coronary artery origin, myocarditis and long QT syndrome) that could cause sudden death in young athletes
• One survey of young athletes revealed that 6.2% reported a previous syncopal episode. Syncope was unrelated to exercise in most cases (86.7%), was post-exertional in 12% and was exertional in 1.3%
• Tilt table testing to evaluate syncope and presyncope in young athletes is to be undertaken with caution concerning interpretation as they may have an increased susceptibility to greater vagal tone leading to an increase in false-positive findings and inappropriate reassurance. If a fainting athlete experiences syncope during a tilt table test, this may not be the cause of the presenting syncope. The patient should be asked if the tilt table test produced symptoms similar to the presenting syncope. Cardiac causes may still need to be considered.

Further reading on Sudden Cardiac Death (SCD) in athletes

• Recommendations for participation in competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and pericarditis: position statement of the sport cardiology section of the European Association of Preventive Cardiology (EAPC), European Heart Journal, Pages 19-3
• Eligibility and disqualification recommendations for competitive athletes with cardiovascular abnormalities - scientific statement from the American Heart Association and American College of Cardiology. J Am Coll Cardiol 2015 Dec 66 (21) 2343 - 2349
• FIFA player health programme: how to prevent sudden cardiac death in football resource for players to highlight the warning signs and causes of sudden cardiac death in athletes.

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Exercise-related syncope

History remains key in evaluating exercise-related syncope and key questions include enquiring about previous syncope, palpitations and presyncope related to exercise, and family history of cardiac disease or sudden cardiac death in a young person (under 40 years). Points to consider:

• It is important to distinguish between syncope occurring during exercise and syncope occurring after exercise
• Syncope which occurs during exercise could suggest underlying structural heart disease and may be the only symptom preceding sudden cardiac death
• Syncope occurring after exercise is more likely to be a vasovagal episode due to lack of venous return to the heart, dependent venous pooling and impairment of cardiac baroreceptors
• On occasion syncope after exercise can be due to a cardiac cause
• Guidelines suggest obtaining an ECG in all patients with exercise-related syncope.

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Screening

Key points about athlete screening:

• An Italian national screening programme in young athletes consisting of initial history examination and ECG has reported a 90% reduction in SCD
• Screening programmes using combinations of questionnaire, physical examination, ECG and ECHO have been shown to reveal a 2-4% rate of abnormalities requiring further testing, with a rate of clinically significant abnormalities in about 0.3% of athletes
• The American Heart Association Council on Nutrition, Physical Activity and Metabolism proposed a 12 step screening process aimed at preventing SCD in athletes

• The value of the ECG in screening is uncertain as many disorders that can cause sudden cardiac arrest in athletes will not be detected on a standard ECG, and the variability of ECG interpretation is high
• One study found that six out of eight sudden cardiac deaths had normal screening investigations including history, examination, ECG and echocardiography.   

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The role of the GP in preventing sudden cardiac death in athletes

'Increasing awareness about sudden cardiac death in athletes among general practitioners and primary care providers is an important step in helping to prevent events. Recognition of clinical features and symptoms that may indicate the presence of an underlying cardiac condition and the need for early referral to a cardiologist are essential for early diagnosis and initiating appropriate action'. (BMJ, 2015)

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Falls and syncope

• Syncope and falls increase with age. Contributing factors include changes in body physiology, dehydration and increased mediation use
• 25% of older people will fall each year, and a fifth of these falls will cause serious injury such as a fractured hip or traumatic brain injury
• There is strong consensus that the management of unexplained falls should be the same as that for unexplained syncope
• Non-accidental falls (NAF) may represent under reporting of syncope, or present as syncope in older age groups.

Amnesia associated loss of consciousness (A-LoC)

• A-LoC associated with syncope is a key factor in unexplained falls, especially in older adults. In one study, forty-two per cent of patients over 60 years of age experienced A-LoC post-tilt table induced syncope - they had no recollection of having fainted
• To compound this problem, witness accounts are only be available in just over half of older people experiencing syncope
• Impaired cognitive function and blood pressure changes do not seem to be risk factors for A-LoC.

Carotid Sinus Syndrome (CSS) and A-LoC

• It is reported that 30% of patients with carotid sinus syndrome have A-LoC
• In patients with unexplained falls 95% had A-LoC during CSS and 27% who presented with syncope had A-LoC
• This again illustrates the difficulty in assessing patients who may lack warning symptoms and witness accounts for the event.

Vasovagal syncope (VVS) and A-LoC

• Although the first peak of incidence of VVS occurs in teenagers, up to 40% of unexplained recurrent syncope in older individuals is due to VVS, constituting the second peak.(134) The lower reported prevalence of VVS in the older population may be attributable to a lack of prodromal symptoms, unavailable witness accounts, or the presence of cognitive deficits
• One trial suggests a prevalence of A-LoC with vasovagal syncope of 28%, with increasing age associated with a higher prevalence of A-LOC but a significant proportion (20%) of younger patients are also affected by A-LOC
• Patients with A-LOC and VVS are more likely to have had a fracture associated with a syncopal episode or unexplained fall in the past
• NICE guidance Falls Assessment and prevention of falls in older people.

Read Falls and syncope case histories

Falls and syncope case histories

• Syncope with multiple causes
• Unexplained falls

Case histories - Falls and syncope

• Syncope with multiple causes
• Unexplained falls

Syncope with multiple causes

History

An 80 year old lady awakes in the night needing to pass urine. She stands up from her bed, feels hot and dizzy, takes a few steps then collapses on the floor. Her husband hears her fall and finds her unconscious. She regains consciousness quickly but has no recollection of having fainted and assumes she has tripped. An ambulance is summoned, and she is transported to A+E. She is found to have suffered a Colles fracture, which is reduced and immobilised before she is discharged the following morning.

10 days later she faints again when she rises to go to the toilet in the night. Her husband helps her back to bed and the following day requests a visit from you, the GP. You note a history of hypertension, type 2 diabetes mellitus and overactive bladder. She is taking 12 different medications, notably amitriptyline for her arthritic back and to help her sleep, oxybutynin for incontinence, and 3 antihypertensive drugs (amlodipine, ramipril and furosemide). She reports feeling intermittently dizzy in the day during the past months.

Examination

Cardiovascular examination reveals a heart rate of 86 bpm and BP of 160/95 whilst sitting, which falls to 120/60 with associated dizziness after 2 minutes of standing.

Which investigations should be performed in primary care?

An ECG should be performed and in this case shows borderline left ventricular hypertrophy. Blood tests may be useful in the presence of polypharmacy to check her electrolytes as she is taking a diuretic and ACE inhibitor.

What would you do next?

The key feature in this case is polypharmacy in the context of frailty contributing to syncope. General advice should be given regarding fluid intake and postural manoeuvres to prevent fainting, such as rising from bed slowly and tensing arm and leg muscles before standing (which may offer less benefit in the elderly compared with young people due to the lack of muscle bulk and power). A medication review is important, and you stop her amitriptyline, oxybutynin and furosemide. You establish that she does not drive.

Outcome

You review her 4 weeks later and she reports no further blackouts and her bladder symptoms have improved since discontinuing the diuretic.

Learning points

• Syncope in the elderly is often multifactorial. Causes include impaired autoregulation of blood pressure due to age, polypharmacy, dehydration and comorbidities (e.g. autonomic neuropathy of diabetes).
• Culprit drugs include antihypertensives, diuretics, anticholinergics and tricyclic antidepressants.
• Syncope can masquerade as falls, especially in older people, as patients often have amnesia for syncope.
• A combination of hypertension and orthostatic hypotension can be difficult to manage.

Read the Falls and syncope section of syncope toolkit

Unexplained Falls

History

A 78 year old man consults with you with a history of recurrent falls. He does not recall the events surrounding the falls and has been found on the floor by his carers at home on 3 occasions. He has a past medical history of prostate cancer and is not taking any medication.

Examination

Cardiovascular examination is normal and postural blood pressure measurements show no significant drop.

What would you do next?

He is further investigated with an ECG, FBC and U+E, which are all normal. You refer him to the local falls clinic.

Outcome

He is reviewed by a care of the elderly consultant who organises carotid sinus massage, echocardiogram and Holter monitoring which are all normal. He undergoes tilt table testing and after 6 minutes  he experiences a syncopal episode, with a  heart rate and blood pressure drop. He recognises this to be similar to when he has his falls. He is given advice regarding postural counter-manoeuvres, adequate fluid intake and a healthy diet, refraining from refined carbohydrates to avoiding post-prandial hypotension. There is a reduction in the frequency of syncopal episodes; he is able to recognise presyncope symptoms and he takes avertive action (such as sitting or lying down promptly) to avoid loss of consciousness.

Learning Points

• Vasovagal syncope with amnesia is a cause of recurrent "unexplained" falls in older patients.
• Other common causes of syncope in older patients include orthostatic hypotension and carotid sinus syndrome.
• Holter monitoring is often requested to investigate syncope in secondary care but is unlikely to identify the cause of syncope unless the episodes are extremely frequent.

Read the falls and syncope section

Syncope case histories

Case histories in this toolkit:

Vasovagal syncope

• Carotid sinus syndrome (CSS)
• Convulsive syncope
• Vasovagal syncope
• Post-exercise induced neurally-mediated syncope

Cardiac syncope

• Drug induced bradycardia
• Hypertrophic obstructive cardiomyopathy
• Long QT syndrome
• Myocardial Ischaemia
• Pulmonary embolism
• Aortic stenosis
• Atrial fibrillation
• Brugada syndrome

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Falls and syncope

• Syncope with multiple causes
• Unexplained falls 

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Investigations

• Syncope of unknown origin

Syncope in children and young people

• Anomalous origin of left coronary artery in a child with syncope

Orthostatic hypotension

• Orthostatic hypotension and autonomic neuropathy
• Orthostatic hypotension after squatting case history

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Postural tachycardia syndrome (PoTS)

• Postural tachycardia syndrome (PoTS) case history

Non-haemodynamic collapse / Psychogenic Pseudosyncope (PPS)

• Non-haemodynamic collapse / Psychogenic Pseudosyncope (PPS) case history

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Syncope case histories references (411 KB PDF)

Information for commissioners

The health, social and economic burden of syncope for patients

Compared with people without syncope, those with syncope may experience the following:

The NHS syncope burden

Cost of syncope to the NHS

Much of the information regarding costs of hospital attendance, admission and investigation of syncope patients has been undertaken in secondary care settings and there is little information regarding syncope costs of management in primary care.

Key facts:

• 1-1.5% of A&E attendances are for syncope; 50% of patients are admitted to hospital
• 36% of patients experience significant trauma
• After attending A&E with syncope, 0.7% of patients die in the next 7-30 days, and 10% within a year
• Hospitalisation accounts for over 75% of the costs; most admissions are not necessary
• In a UK-based study, 25% of the patients had more than 20 tests, and 10% had more than 31 tests done
• Patients visit on average 3 different specialists and have 13 inconclusive tests before diagnosis.

Syncope care pathways

Download syncope pathway for primary care (76 KB PDF)

Syncope and Blackout clinics

Services available and referral procedures will differ throughout the UK.

Rapid Access Blackouts Units will usually see patients with both syncopal and non-syncopal causes of transient loss of consciousness  (TLoC). Rapid Access Blackouts Clinics are often staffed by a multidisciplinary team of specialist nurses from backgrounds including cardiology, neurology and medicine for the elderly.

Syncope Units are usually based in secondary care. They can be led by any clinician with an interest in syncope such as cardiologists, A&E consultants and medicine for the elderly. A number of successful services are primarily nurse-led. Some clinics are virtual.

Some syncope clinics will also see patients with recurrent presyncope and PoTS.

• Referral to the unit may be from primary care, A&E, inpatient and outpatient secondary care and occasionally be self-referral
• It is recommended that rapid access referrals can be made for high risk patients
• Rapid access referrals from A+E can also be beneficial for low and intermediate risk patients to reduce hospital admission rates.

Syncope units can reduce healthcare costs primarily by:

• Reducing the number of admissions
• Reducing the duration of hospital stay
• Reducing the number of unnecessary tests.

Useful resources for commissioners

• Syncope Unit: rationale and requirement - the European Heart Rhythm Association position statement endorsed by the Heart Rhythm Society (2015)
• Blackout Care Pathways
• Healthcare Pioneers Report - showcasing best practice in syncope.