Syncope
From Ganfyd
Contents |
Introduction
Syncope while commonly understood as a temporary loss of consciousness owing to generalised cerebral ischaemia, is strictly any (sudden) loss of consciousness from generalised cerebral ischaemia.
With regard to assessing reversible syncope, some important points are:
 | Measure the postural BP ie lying vs standing. A drop of more than 20mmHg suggests poor autoregulation eg vasovagal but not very sensitive |
- The history is extremely important. The setting and the immediate events before, during and after the event are crucial to differentiate the many causes. An eye witness account is invaluable and in difficult cases with the patient's consent it is well worth striving to obtain. This can be to the extent of phoning a witness when taking the history from the patient in clinic.
- Drug history - diuretics, antihypertensives etc.
- Jerks do not necessarily imply epilepsy - anoxic myoclonic seizures may accompany any cause of cerebral ischaemia.
If the syncope occurred in a situation likely to pertain while driving then the patient should be advised to inform the DVLA and not to drive.
- Vasovagal syncope is probably the most common cause and is often obvious from the history/examination - needs no further assessment.
- A dangerous cardiac arrhythmia should be considered where syncope is triggered by exercise or accompanied by chest pain/palpitations
Aetiology
Any medical condition or pathology that can cause sudden and profound global cerebral ischaemia could be responsible. The underlying mechanisms involve either a fall in perfusion below that necessary for cerebral function or hypoxia. In practice given human physiology the three seconds odd of global cerebral ischaemia necessary to produce loss of consciousness are more likely to involve circulatory dysfunction than hypoxia, with the notable exception of a toxin for aerobic metabolism. Certainly spontaneously recoverable syncope is most likely to involve the former.
Common Causes
- Vasovagal syncope or neurocardiogenic syncope is the common faint associated with a stress response of the autonomic nervous system which can either suddenly lower the pulse rate, the blood pressure or both together. It is one of the neurally-mediated reflex syncopes which can have either a reasonably pure cardioinhibitory response, baroreceptor response or mixture of the two. There is fair evidence that the cardioinhibitory response is independent of the baroreseptor response and generally precedes it by a few seconds.
- Carotid sinus syncope, also known as carotid sinus syndrome is associated with abnormal sensitivity to external pressure over the region of the nerve sensory organ at the bifurcation of the external and internal carotid arteries in the neck. Another reflex syncope.
- Orthostatic hypotension Falls in blood pressure when standing can result from
- Autonomic failure owing to diabetes, drugs or multiple systems atrophy
- Hypotensive effects of drugs including alcohol, and all drugs used to treat hypertension and a fair few for other conditions, such as dopaminergic drugs used to treat parkinsonism and thalidomide for multiple myeloma
- Volume depletion such as in massive haemorrhage or profuse diarrhoea.
- cardiac arrhythmia
- Any asystole of the order of 3 seconds, with complete heart block or sinus bradycardia aggravated by drugs (eg beta blockers) being the most common
- Any tachycardia with loss of effective ventricular contraction, with ventricular tachyarrhythmias in the context of ischaemic heart disease being the most common
Causes always to be considered as underlying condition common and treatable
Rarer Causes
- Tussive syncope induced by coughing fits, also called laryngeal syncope.
- Laughter-induced syncope.
- Micturition syncope, defaecation syncope
- Post prandial syncope
- Structural heart disease
- Impaired circulation
- Tumour causing pressure on vena cava
- Pregnancy
- A-V shunt
- Arterial steal syndrome
- Cerebral vasoconstriction syndrome - a type of reflex syncope
- Tumour causing pressure on carotid sinus
Symptoms
- Loss of consciousness
- Sudden loss of balance
- Unexplained fall/collapse
Differential Diagnosis
Although syncope is not in itself a diagnosis, the following conditions may cause confusion leading to inappropriate management or visa versa.
- Intoxication
- Metabolic disorders causing hypoglycaemia
- Sleep apnoea
- Neurological Conditions
- Transient ischaemic attacks (TIA) of carotid origin
- Vertebro-basilar transient ischaemic attack
- Epilepsy
- Narcolepsy
- Drop attacks
- Explained Falls
- Psychogenic pseudosyncope
Diagnosis
Features Suggestive of Syncope
- New pain, unpleasant sight, sound, smell or situation -vaso-vagal syncope, but if chest pain cardiac syncope/PE
- Long history of syncope
- On standing - orthostatic hypotension
- Relationship to initiation or change of dose in beta blocker, antiarrhythmic, hypotensive agent (includes vasodilators, thalidomide and dopaminergic drugs) or drug that will interact with other such drugs - orthostatic hypotension, cardiac arrhythmias- aortic stenosis
- Standing for prolonged periods- orthostatic hypotension
- Standing in crowded, hot places - vaso-vagal syncope
- Nausea, vomiting associated with syncope - vaso-vagal syncope
- After/during a meal - post prandial syncope
- On head rotation, pressure on neck from tumours, shaving, tight collars - carotid sinus syncope
- After exertion, isometric exercise- arrhythmias/strucural cardiac/situational syncope
- Diabetes with neuropathy or atypical parkinsonism - orthostatic hypotension from autonomic neuropathy
- Palpitations before- arrhythmias
- Family history - vaso vagal syncope
- History sudden death - arrhythmias
- Evidence structural heart disease - cardiac syncope
- Arm exercise - steal syndrome
- ECG evidence of
- Sinus bradycardia (<50 bpm), > 3 second pause, Mobitz type 1 second degree a-v block, sinoatrial block
- Bifascicular block or other intraventricular conduction abnormalities (QRS duration greater than 0.12 s)
- Pre-excitation (delta waves)
- Prolonged QT interval
- Changes suggesting acute myocardial infarction
- Note the above is not exhaustive, but rare conditions such as Brugada syndrome and arrhythmogenic right ventricular dysplasia will have ECGs that meet the above descriptions.
History
With vasovagal syncope, there is usually a prodrome of dizziness, nausea, tunnel vision and pallor. Such symptoms may have occurred previously without progressing to syncope. The trigger is usually standing up after a prolonged period of sitting/lying, but it can also occur with prolonged sitting. A complete and verified history from independent sources is necessary for accurate diagnosis. It has been shown that unexplained falls in the elderly are often caused by syncope, emphasising that patients can fail to recognise syncope or its prodrome. There may or may not be loss of consciousness. An anoxic seizure may follow immediately after the collapse, which is not epileptic (an EEG would show flattening rather than spikes/waves), and tends to be characterized by stiffening, posturing and fine twitching or myoclonus lasting a few seconds only. Warning signs in the history suggesting something more sinister include:
- Chest pain
- Syncope during exercise
- Syncope while supine
- Family history of sudden death in young person
- Odd history
- Unusual age group ie young child or new onset late in life
Syncope can be polyfactorial. The incidental hint of major surgery a few weeks before symptoms started can lead to the diagnosis of multiple pulmonary emboli, as can the more common change in drug therapy a few days before symptoms started.
Examination
A directed but thorough examination emphasizing the cardiovascular examination but not neglecting the neurological or say abdominal (pelvic tumour impairing venous return) is indicated. The rate, rhythm and character of the pulse should be assessed and the presence or absence of murmurs, heave and peripheral pulses recorded. Orthostatic blood pressure measurements should be done and affect diagnosis in about quarter of cases, even if done by real life clinicians in only 38% of presentations[1]. Carotid sinus massage should not be done without ECG monitoring and the 1/1000 odds of precipitating embolic cerebrovascular symptoms in the elderly with atheroma in the two large series published to date should not be forgotten.
Investigations
This is a condition in which it may be particularly tempting to order costly tests that will add little or nothing to the management. One American study demonstrated massive resource waste in inappropriate electroencephalography, CT scans, and cardiac enzymes tests[1]
Do an ECG, which is cheap and non-invasive. Possible findings include:
- Long QT interval - age specific normals available for children but unlikely to be significant under 500ms
- Pre-excitation viz short PR (under 15ms) or delta wave
- Heart block
- Ventricular hypertrophy
A normal ECG and physical examination define a good prognosis group in terms of mortality. Clear vasovagal syncope might not even require an ECG, and certainly does not require further investigation. Other initial investigations would be guided by clinical presentation and indeed should be based mainly on the need from the particular presentation to exclude non-syncope causes of loss of consciousness. Unhappily these and non urgent investigations are all too often done in a haphazard manner, with considerable waste of resources. Glucose (to exclude hypoglycaemia), electrolytes, and arguably a full blood count (to exclude anaemia). At least one patient has presented with a normal ECG and complete retrospective denial of chest pain, although the history from his wife motivated a repeat ECG and troponin measurement which confirmed a myocardial infarction as the cause of syncope, so it is difficult to be proscriptive.
A suspicion of paroxysmal tachyarrhythmia should lead to prolonged ECG monitoring, with or without event recording. Exertion related symptoms should be investigated with an exercise test. If and only if there is evidence for structural heart disease should an echocardiogram be obtained.
Tilt table studies should be done on those with recurrent syncope and a normal ECG, particularly where there is suspicion of neurally mediated symptoms. Can be done from the age of 6yrs onwards (younger children get bored). Positive responses are:
- Asystole
- Paradoxical bradycardia or else unresponsive heart rate in the presence of hypotension
Where symptoms are induced without changes in heart rate and blood pressure, then simultaneous EEG or cerebral blood flow monitoring may give the diagnosis of cerebral vasoconstriction syndrome.
Carotid sinus massage should be done on the elderly or those where neck movements could have been associated with syncope. This may be combined with the tilt table study most effectively, but is likely to be contraindicated in those with evidence of carotid territory cerebrovascular disease.
Iron deficiency with/without anaemia is associated with neurocardiogenic syncope, though it is not yet proven that supplementation helps [2]
Consider admission to hospital for continuous ambulatory ECG and EEG monitoring if syncope is occurring several times a day every day. If no abnormality of monitoring or BP/HR during episodes then the diagnosis of psychogenic pseudosyncope is suggested.
Treatment
Education
Patients and relatives commonly appreciate a full and reassuring explanation of vasovagal syncope with its usually benign prognosis.
The removal of addressable precipitants is always the first step. This includes for example tight collars with carotid sinus syncope. Fluid intake should be optimized, and salt supplementation may be appropriate eg for athletes.
There are manoeuvres that can be employed when standing such as crossing legs, folding arms, shifting weight from heels to toes and back if periods of prolonged standing cannot be avoided.
Drug therapy
There is little good quality evidence to guide therapy. There is likely to be significant placebo effect.
- Midodrine. This alpha adrenoreptor agonist has proven effectiness but while licensed in many countries has never been marketed in the U.K.
- betablockers, although widely used do not have a strong evidence base for effectiveness.
- Plasma expanders such as fludrocortisone and NSAIDs can work with orthostatic hypotension, and might work with baroreceptor mediated syndromes
Surgery
- Pacing is indicated for heartblock less than 40/min or asystole lasting 3 seconds generally and a severe cardioinhibitory response of this magnitude to carotid sinus massage or tilting.
External Links
- 2004 European Society of Cardiology Guidelines on Management (Diagnosis and Treatment) of Syncope.
- McLeod KA. Syncope in childhood. Archives of disease in childhood. 2003 Apr; 88(4):350-3.
References
- ↑ a b Mendu ML, McAvay G, Lampert R, Stoehr J, Tinetti ME. Yield of diagnostic tests in evaluating syncopal episodes in older patients. Archives of internal medicine. 2009 Jul 27; 169(14):1299-305.(Link to article – subscription may be required.) (see also A J Calderon. Time to Abandon the "Shotgun Approach" to Syncope Evaluation (comment on Mendu ML et al article). 2009 Journal Watch. Last updated: 31 August 2009. Last viewed 2 September 2009.)
- ↑ Jarjour IT, Jarjour LK. Low iron storage in children and adolescents with neurally mediated syncope. The Journal of pediatrics. 2008 Jul; 153(1):40-4.(Link to article – subscription may be required.)
