Postgrad Med J 2001;77:99–102 99 Postgrad Med J: first published as 10.1136/pmj.77.904.99 on 1 February 2001. Downloaded from Important points in the clinical evaluation of patients with syncope W Arthur, G C Kaye A careful history, physical examination, and an diagnosis for syncope varies with age; this fact electrocardiogram (ECG) are the most impor- coupled with other historical findings can help tant components of the evaluation of a to pinpoint the diagnosis (table 1). syncopal episode. These three components will provide a diagnosis or determine whether diag- PRODROMAL SYMPTOMS nostic testing is necessary in most patients.1 Most persons with neurocardiogenic syncope The potential cost savings made by avoiding have premonitory symptoms before losing unnecessary and expensive investigations are consciousness; usually nausea, diaphoresis and obvious when one considers that good clinical pallor.3 Yawning, visual blurring, weakness, skills lead to the identification of the cause of and a feeling of impending doom are consistent syncope in 75%–85% of cases in which a suc- with neurally mediated syncope. The presence cessful diagnosis is made.2 of palpitations preceding syncope is highly suggestive of an arrhythmia. Syncope caused History by ventricular tachycardia typically occurs A comprehensive account of the events preced- without a prodrome, although some patients ing the syncopal spell is invaluable for diagno- may report brief palpitations, with light head- sis (box 1). The premonitory (prodromal) edness preceding loss of consciousness. Su- symptoms, precipitating factors, rate of onset, praventricular tachycardia may occasionally witnessed accounts, features during the recov- lead to loss of consciousness; in these rare cases ery phase, past medical history, and the palpitations are frequently noticed by the frequency and previous history of syncope will patient.4 A characteristic aura immediately assist in the diagnosis and direct the physician preceding syncope might implicate epilepti- in the evaluation of patients. The diVerential form activity. Box 1: History preceding syncope PRECIPITATING FACTORS x Neurally mediated syncope Syncope on exertion implies left ventricular Premonitory symptoms: pallor, diaphore- outflow tract obstruction, left ventricular dys- sis, nausea, visual blurring, light function, or ventricular dysrrhythmia. Loss of headedness, hearing loss consciousness after the completion of exercise Situation: neck turning, stress, pain, fear, maybe due to a strong vagal response produc- crowding, prolonged upright posture, ing a significant bradycardia. Sudden symptom http://pmj.bmj.com/ cough, micturition, swallowing, defecation onset unrelated to posture or eVort is sugges- Castle Hill Hospital, tive of a cardiac arrhythmia. Coexistent sudden Castle Road, East x Cardiac syncope Yorkshire, UK Abrupt onset, eVort, or exertion, preced- onset pleuritic chest pain and/or dyspnoea may W Arthur ing chest pain, palpitations indicate a pulmonary embolism. Diagnosis of GCKaye Drug related arrhythmia: antiarrhythmics, carotid sinus syncope requires that spontane- neuroleptics, digoxin, â-blockers, alcohol, ous symptoms of presyncope or syncope be Correspondence to: reproduced by carotid sinus massage.5 Correla- Dr Wayne Arthur, illicit drugs on September 25, 2021 by guest. Protected copyright. Department of Cardiology, x Orthostatic syncope tion between symptoms and precipitating Peterborough District Abrupt changes in posture factors such as neck twisting, wearing a tight Hospital, Thorpe Road, collar, shaving, or previous neck surgery Peterborough PE3 5DE, UK Drug related: angiotensin converting wayne@ enzyme (ACE) inhibitors, nitrates, diuret- reinforces the diagnosis. Syncope occurring denecres.freeserve.co.uk ics, alcohol after abrupt changes in posture would impli- cate orthostatic syncope. This diagnosis may Submitted 30 December Postprandial 1999 Haemorrhage frequently be missed due to concurrent hyper- 6 Accepted 16 February 2000 tension in the supine position. Postprandial hypotension and even syncope may occur as a Table 1 Age distribution of syncope consequence of splanchnic shunting of blood and the intake of alcoholic beverages.7 Epi- Young (<35 years) Middle aged (35–65 years) Elderly (>65 years) sodes related to stressful or emotional situa- Neurally mediated: Neurally mediated Cardiac: tions point towards neurally mediated syncope; Neurocardiogenic Arrhythmic in these circumstances the patient is often Cardiac: Mechanical aware of losing consciousness. Psychiatric Arrhythmic Mechanical Orthostatic: [Hypertrophic Drug induced WITNESSED ACCOUNTS cardiomyopathy] In addition to the history given by the patient [WPW syndrome] Neurally mediated: information available from an observer of the Carotid sinus hypersensitivity event is crucial. The duration of syncope is by [Long QT syndrome] definition, transient. After a seizure loss of [ ] indicates less common but important causes of syncope. WPW = WolV-Parkinson-White. consciousness may be prolonged. Full assess- Reproduced with permission from Olshansky.17 ment of the patient is not complete until eye www.postgradmedj.com 100 Arthur, Kaye Postgrad Med J: first published as 10.1136/pmj.77.904.99 on 1 February 2001. Downloaded from witness accounts of the events preceding and neurocardiogenic syncope. Ophthalmic prepa- following the patient’s loss of consciousness are rations, mostly â-blockers, can aggravate brady- taken from those accompanying the patient to arrhythmias or heart block. Antiarrhythmics, the emergency department or the clinic. If the antidepressants, psychotropic drugs, many patient is unaccompanied at initial presenta- non-sedating antihistamine drugs, and other tion potential witnesses should be encouraged preparations may independently, or interact to, to attend as they may hold the clues to the prolong the QT interval predisposing to diagnosis. It must be remembered of course polymorphic ventricular tachycardia. that witnessed accounts, while often heavily relied upon, may be inaccurate. MISCELLANEOUS POINTS RECOVERY PHASE Patients with a family history of syncope or The account of the observer is particularly sudden death raise the possibility of the invaluable when trying to diVerentiate between congenital long QT syndromes, hypertrophic types of syncope and seizure. The presence of cardiomyopathy or WolV-Parkinson-White confusion after the event is the single most syndrome. There may be a familial history of powerful discriminator between seizure and neurocardiogenic syncope. A detailed family syncope.8 Mental function is usually quickly history should therefore be taken including recovered after a syncopal episode, whereas data relating to distant relatives who died seizures are followed by a postictal period of unexpectedly and any relevant familial disease. residual confusion which can last from minutes A psychiatric history may reveal anxiety disor- to hours. DiVerentiating the recovery time ders, major depression, and hysterical person- between causes of syncope is more diYcult but ality disorder. Patients with syncope and recovery after neurocardiogenic syncope can psychiatric disorders are younger (more often take minutes in comparison with postural female), have a high number of syncopal hypotension or a long sinus pause after which episodes and have a variety of other com- the patient is alert within seconds. Dizziness or plaints. In young patients with no structural headache in the recovery phase (in the absence heart disease those with multiple episodes of of head trauma) points towards a neurological syncope (>5 in preceding year) are less likely to cause. have an arrhythmia and are more likely to have psychiatric illnesses.11 A full social history is PAST MEDICAL HISTORY also important to exclude illicit drug use as a The patient with depressed left ventricular cause of syncope and to pinpoint risk factors function and/or ischaemic heart disease in for ischaemic heart disease. The occupation of association with syncope is at high risk of sud- the patient is essential information as urgent den death.9 Obtaining a cardiac history and diagnosis and therapy is required in those elucidating associated risk factors for ischaemic whose careers and safety are compromised by heart disease is mandatory during clinical syncope. evaluation. The presence of diabetes mellitus frequently causes silent myocardial ischaemia Physical examination http://pmj.bmj.com/ and may mask a myocardial infarction giving During a thorough physical examination atten- rise to a ventricular arrhythmia. Diabetic tion should be directed to the vital signs, the peripheral neuropathy may also lead to orthos- cardiovascular and neurological examination. tatic syncope. Features suggestive of multiple After a supine period of at least five minutes system atrophy may be elicited from the history blood pressure and pulse measurements in patients with orthostatic syncope. should be taken; these should be repeated after Risk can be assessed at the initial presenta- the patient has been standing for three on September 25, 2021 by guest. Protected copyright. tion by examining the frequency of syncope. If minutes. An abrupt drop in systolic blood recurrent episodes are spread out over a pressure of between 20–30 mm Hg with stand- number of years malignant arrhythmias are ing associated with reproduction of symptoms unlikely to be the cause. Multiple syncopal suggests orthostatic syncope as a cause.12 In a recurrences are most likely due to neurally volume depleted