Important Points in the Clinical Evaluation of Patients with Syncope

Home , Orthostatic syncope, Syncope (medicine)

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 implicate 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 patient the heart rate should mediated syncope or psychiatric causes. In rise on standing. In those with dysautonomic contrast, patients with isolated (<3) episodes of syncope the blood pressure can drop over sev- syncope or with a short history of recurrence eral minutes while upright with no concomi- are at risk of cardiac death.10 New onset tant change in heart rate. syncope may herald a new serious cardiovas- Because the prognosis after syncope is worse cular cause. if there is underlying cardiac disease, the prin- cipal objective of the examination is to DRUG HISTORY determine whether there is evidence for under- Medications, particularly in the elderly, may be lying cardiovascular abnormality. The cardio- causal for syncope in a substantial number of vascular examination may reveal a pulse patients. A detailed drug history should be character or murmurs consistent with left ven- taken; in particular changes in medication or tricular outﬂow tract obstruction. Mitral valve the initiation of a new drug maybe implicated prolapse, left atrial myxoma, pulmonary hyper- in the aetiology of the event. Antihypertensives, tension, or prosthetic valve dysfunction may nitrates, and diuretics are frequently contribu- also be suspected after auscultation of the pre- tory to orthostatic hypotension. Vasodilatation cordium. A third or fourth heart sound and/or volume depletion may trigger enhanced consistent with cardiac disease and/or conges- central mechanoreceptor responses leading to tive cardiac failure may be heard.

www.postgradmedj.com Clinical evaluation of patients with syncope 101 Postgrad Med J: first published as 10.1136/pmj.77.904.99 on 1 February 2001. Downloaded from In the absence of contraindications (carotid bruit, stroke, or myocardial infarction within Summary points the previous six months, or a history of x The history and examination are the ventricular tachycardia or ventricular ﬁbrilla- most important stages involved in strati- tion) carotid sinus massage (CSM) should be fying the patient into high and low risk performed in all individuals with unexplained groups and identifying the cause of syn- syncope, particularly those who are elderly cope. with features suggestive of carotid sinus x Those with a history of structural or syncope.13 14 Massage to the carotid sinus is ischaemic heart disease or with recent performed by applying longitudinal digital onset, isolated episodes of syncope have pressure at the bifurcation of the internal and a high risk of sudden death. external carotid artery for ﬁve seconds. CSM is x Obtaining an eyewitness account is a applied to the right then the left side after a two vital component of the initial assess- minute interval. Pressure should never be ment of the cause of syncope. Postural hypotension and carotid sinus applied to both sides simultaneously. A stand- x syncope can be reliably and safely diag- ard technique of carotid sinus stimulation with nosed at the time of examination if a applied exclusion criteria, as outlined above, standard technique is adhered to. causes infrequent complications most of which x An abnormal ECG is found in up to are transient and result in full recovery.14 50% of patients with syncope and Potential complications of CSM include ven- should therefore be part of the initial tricular arrhythmias and prolonged asystole, clinical assessment. therefore continuous ECG monitoring and venous access is required. Pulmonary examination and assessment of Conclusion the jugular venous pressure may reveal conges- When a cause of syncope is determined, it is tive heart failure. The response to voluntary most frequently established on the basis of hyperventilation may be useful in certain clinical data available at the time of initial con- patients and has been advocated as part of tact with the physician. A diagnostic strategy 15 standard evaluation of syncope. In the should utilise these data as a guide to further context of an acute syncopal episode a rectal investigation thereby minimising costly proce- examination should be performed to look for dures that may ultimately be misleading. Such evidence of an occult gastrointestinal bleed. a strategy requires a thorough account of the The neurological examination should look to episode(s) of syncope from the individual identify focal neurological signs that may oVer aVected and witnesses present. The age of the an immediate diagnosis and redirect investiga- patient is useful to broadly stratify causes of tions accordingly. syncope. The routine ECG is part of the initial clinical assessment and can identify potential Electrocardiogram causes of syncope or patients with structural

An ECG should be performed in all patients heart disease in signiﬁcant numbers. The crux http://pmj.bmj.com/ with syncope. An abnormal ECG is found in of stratifying those at high risk depends on up to 50% of patients with syncope, but in whether or not structural heart disease is most patients it is not diagnostic.16 In a person present. Gaining this information at the earliest with a normal ECG there is a low likelihood possible opportunity should expedite the suc- that an arrhythmia is the cause of syncope, and cessful management of the patient. these persons are at low risk of sudden death.11 Despite being a brief investigation the ECG 1 Linzer M, Yang EH, Estes NA 3rd, et al. Diagnosing

syncope. Part 1: value of history, physical examination, and on September 25, 2021 by guest. Protected copyright. together with a rhythm strip can identify electrocardiography. Clinical eYcacy assessment project of potential causes of syncope in 2%–11% of the American College of Physicians. Ann Intern Med 16 1997;126:989–96. patients. Acquired or congenital disease of the 2 Day SC, Cook EF, Funkenstein H, et al. Evaluation and atrioventricular node or the distal conduction outcome of emergency room patients with transient loss of consciousness. Am J Med 1982;73:15–23. (His-Purkinje) system may be evident from 3 Calkins H, Shyr Y, Frumin H, et al. The value of the clinical second or third degree heart block. There may history in the diVerentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic be evidence of conduction system disease in syncope. Am J Med 1995;98:365–73. the His-Purkinje system with a prolonged P-R 4 Leitch JW, Klein GJ, Yee R, et al. Syncope associated with supraventricular tachycardia: an expression of tachycardia interval and associated bundle branch block rate or vasomotor response? Circulation 1992;85:1064–71. and fascicular block. This pattern might impli- 5 Hammill SC. Value and limitations of noninvasive assessment of syncope. Cardiol Clin 1997;15:195–218. cate intermittent complete heart block as a 6 Robertson D, Robertson RM. Causes of chronic orthostatic cause of syncope and give a clue to underlying hypotension. Arch Intern Med 1994;154:1620–4. 7 Lipsitz LA, Ryan SM, Parker A, et al. Hemodynamic and structural heart disease. The presence of autonomic nervous system responses to mixed meal bundle branch block increases the likelihood ingestion in healthy young and old subjects and dysautonomic patients with postprandial hypotension. Circulation that significant sustained monomorphic ven- 1993;87:391–400. tricular tachycardia will be inducible at electro- 8 Gastaut H, Fischer-Williams M. Electroecephalographic 17 study of syncope: its diVerentiation from epilepsy. Lancet physiological testing. The ECG may indicate 1957;ii:1018–25. sinus node dysfunction, myocardial infarction, 9 MiddlekauV HR, Stevenson WG, Saxon LA. Prognosis after syncope: impact of left ventricular function. Am Heart J ventricular pre-excitation, or a long QT 1993;125:121–7. 10 Krol RB, Morady F, Flaker GC, et al. Electrophysiological interval. The electrical criteria for left ventricu- testing in patients with unexplained syncope: clinical nonin- lar hypertrophy may be fulfilled raising the sus- vasive predictors of outcome. J Am Coll Cardiol 1987;10: picion of left ventricular outflow tract obstruc- 358–63. 11 Kapoor WN. Diagnostic evaluation of syncope. Am J Med tion. 1991;90:91–106.

www.postgradmedj.com 102 Arthur, Kaye Postgrad Med J: first published as 10.1136/pmj.77.904.99 on 1 February 2001. Downloaded from 12 Atkins D, Hanusa B, Sefcik C, et al. Syncope and orthostatic 15 Linzer M, Varia I, Pontinen M, et al. Medically unexplained hypotension. Am J Med 1991;91:179–85. syncope: relationship to psychiatric illness. Am J Med 1992; 13 Wagshal AB, Huang SKS. Carotid sinus hypersensitivity. In: 92:18–25. Grubb BP, Olshansky B, eds. Syncope: mechanisms and man- 16 Kapoor WN. Evaluation and outcome of patients with syn- agement. Armonk, NY: Futura, 1998: 281–95. cope. Medicine 1990;69:160–75. 14 Davies AJ, Kenny RA. Frequency of neurologic complica- 17 Olshansky B. Syncope: overview and approach to manage- tions following carotid sinus massage. Am J Cardiol ment. In: Grubb BP, Olshansky B, eds. Syncope: mechanisms 1998;81:1256–7. and management. Armonk, NY: Futura, 1998: 15–71. http://pmj.bmj.com/ on September 25, 2021 by guest. Protected copyright.