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It is important to distinguish between syncope and true vertigo.
The most common cause of syncope is neurally mediated syncope.
A detailed history and physical examination are more useful than extensive investigations.
It is essential to identify high-risk patients for the serious potential cardiac causes of syncope so that appropriate treatment can be given.
A key diagnostic step is to determine whether a central or peripheral cause of vertigo is more likely.
Dynamic manoeuvres may be both diagnostic and therapeutic.
Syncope and vertigo are relatively common symptoms. They are often described by patients using the term ‘dizziness’; however, it is essential to differentiate between the two. Syncope and vertigo both represent a significant diagnostic challenge and it is important to risk stratify patients accurately to distinguish between potentially life-threatening and benign causes.
Syncope as a presenting symptom represents about 1% to 1.5% of all emergency department (ED) attendances. It is a symptom, not a diagnosis. It is defined as a loss of consciousness induced by the temporarily insufficient flow of blood to the brain. Patients recover spontaneously, without therapeutic intervention or prolonged confusion.
There is no simple test to distinguish between the benign and potentially life-threatening causes of syncope, but a careful history, examination and bedside investigations can help to determine appropriate disposition.
The causes of syncope are summarized in Box 8.6.1 . The most common cause in all age groups is neurally mediated syncope, also known as neuro-cardiogenic or vasovagal syncope. Orthostatic hypotension and cardiac causes are the next most common.
Neurally mediated | Cardiac |
---|---|
Vasovagal/neurocardiogenic Situational: cough, micturition, defaecation Carotid sinus syndrome |
Structural valvular disease, such as aortic stenosis Cardiomyopathy Unstable angina Myocardial infarction Bradyarrhythmias, such as sinus node disease, atrioventricular block Tachyarrhythmias, such as ventricular tachycardia, supraventricular tachycardia and torsades de pointes Pacemaker/defibrillator dysfunction Pulmonary hypertension Pulmonary embolus Aortic dissection |
Orthostatic hypotension | Neurological |
Dehydration Vasodilatation |
Vertebro-basilar transient ischaemic attack Subclavian steal |
Medication | Psychiatric |
Anti-hypertensives β-blockers Cardiac glycosides Diuretics Antiarrhythmics Anti-parkinsonian drugs Nitrates Alcohol |
Patients with syncope are often completely asymptomatic by the time they arrive at hospital. A thorough history and physical examination is the key to finding the correct cause of the syncope. The history should focus on the patient’s recollection of the preceding and subsequent events, including environmental conditions, physical activity, prodromal symptoms and any intercurrent medical problems. Accounts from eyewitnesses or first responders are also vital. Medications that may impair autonomic reflexes must be scrutinized and a postural blood pressure measurement performed. Physical examination should concentrate on finding signs of structural heart disease as well as assessing any subsequent injuries.
Neurally mediated syncope causes a typical prodrome: patients complain of feeling light-headed and faint and often describe a blurring or ‘tunnelling’ of their vision. This may be accompanied by other vagally mediated symptoms, such as nausea or sweating. If patients are unable or unwilling to follow the body’s natural instincts to lie flat, they may collapse to the ground as they lose consciousness. This reflex brings the head level with the heart, resulting in an improvement in cerebral perfusion and a return to consciousness. During this time the patient may exhibit brief myoclonic movements, which can be mistaken for seizure activity but, in contrast with true epileptic seizures, there are no prolonged post-ictal symptoms. Fatigue is common following syncope.
Orthostatic hypotension occurs when the patient moves from a lying position to a sitting or standing position. If the required autonomic changes fail to compensate adequately, even healthy individuals will experience light-headedness or a blurring of vision and possibly loss of consciousness. The most vulnerable people are those with blunted or impaired autonomic reflexes, such as the elderly, those on certain medications (particularly vasodilators, antihypertensive agents and β-blockers) and those who are relatively volume-depleted due to heat, excessive fluid losses or inadequate oral intake.
Cardiac syncope is more likely to present with an absent or brief prodrome. Sudden unexplained loss of consciousness should raise suspicion for a cardiac arrhythmia, particularly in the high-risk patient. Both tachycardia and bradycardia can be responsible. A syncopal event while supine is of particular concern and a predictor of a cardiac cause. Syncopal events that occur during exertion should prompt a search for structural heart disease, in particular aortic stenosis.
Most of the published literature on the assessment of patients presenting to EDs with syncope has focused on identifying risk factors for mortality or an adverse cardiac outcome. These assessments include a number of scores and clinical decision rules, such as the Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL) score and the San Francisco Syncope Rule (SFSR). Patients with syncope can be divided into high- and low-risk groups, as shown in Box 8.6.2 . Low-risk patients can be safely discharged for outpatient follow-up, but controversy over high-risk patients remains. It is likely that there is a significant proportion of patients in the high-risk group who actually have an intermediate risk and, given further evaluation in the ED or a short-stay unit, could also be safely discharged; however, it is more difficult to identify this subset.
Chest pain consistent with ischaemic heart disease
History of congestive cardiac failure
History of ventricular arrhythmias
Pacemaker/defibrillator dysfunction
Abnormal electrocardiogram (findings such as prolonged QTc interval, conduction abnormalities, acute ischaemia)
Exertional syncope/valvular heart disease
Age >60 years
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