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Dizzy spells and syncope: investigation and management
Acute care
Dizzy spells and syncope: investigation and management
Relevance to the curriculum 1.0 Good clinical care 1.1 History, examination, diagnosis, record keeping, safe prescribing and reflective practice 7.0 Recognition and management of the acutely ill 7.1 Core skills in relation to acute illness
Neil R Grubb Nicholas A Boon
admissions in the UK.1 Recurrent symptoms are particularly disabling because they affect an individual’s ability to work and to drive, increase susceptibility to falls and associated injuries, and reduce independence in the elderly.
Abstract Dizziness and syncope are common symptoms in the general population, especially the elderly. Syncope can be disabling and result in physical injury and loss of independance. Causes can be divided into arrhythmia, mechanical reduction in cardiac output, inappropriate vasodilatation, neurogenic and metabolic. Patients with cardiac syncope have a poor prognosis unless the cause is quickly identified and treated. The key to making a diagnosis is obtaining a clear history from the patient or a witness of the temporal pattern of symptoms including precipitants, a description of the blackout itself, and speed of recovery. Examination focuses on identification of signs of structural heart disease and postural hypotension. If the history suggests a cardiac diagnosis, echocardiography and ambulatory ECG recording are helpful investigations. For patients with intermittent symptoms suggesting arrhythmia, implantable ECG loop recorders are increasingly used. Tilt testing is used to investigate possible vasovagal syncope, and EEG or MRI head scan can be used to identify potential neurologocal causes of blackouts. Cardiovascular causes of syncope are treated by removal of reversible triggers (e.g. drugs that cause bradycardia or hypotension) or by treatment of the underlying condition (e.g. permanent pacemaker for symptomatic bradycardia, aortic valve surgery for aortic stenosis). Vasovagal syncope is more difficult to treat but can be helped by avoiding identifiable triggers, use of medication and in some cases dual chamber pacing.
Recurrent syncope Syncope is defined as a blackout caused by reduced cerebral perfusion, but can be difficult to distinguish from other causes of loss of consciousness. Recurrent blackouts have four principal mechanisms (Table 1). • Cardiac syncope occurs in patients with structural heart disease or conducting system disease, and also results from a decrease in cardiac output caused by cardiac arrhythmia, valve disease (e.g. aortic stenosis), ventricular impairment or another mechanical problem. Patients with recurrent syncope who have structural heart disease have a poorer diagnosis than any other group. • Inappropriate vasodilatation is the most common cause of recurrent syncope in patients with a structurally normal heart.
Causes of recurrent syncope Arrhythmia • Bradycardia (e.g. sinus node disease, atrioventricular block) • Tachycardia (particularly ventricular tachycardia) Mechanical causes of reduced cardiac output • Extensive myocardial ischaemia/LV dysfunction • Ventricular outflow obstruction (e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy) • Pulmonary embolism • Cough syncope
Keywords arrhythmia; dizziness; ECG/ambulatory ECG; elderly; hypotension; pacemaker; syncope; tilt testing
Dizziness affects about one-third of individuals over the age of 65 years, and is one of the most common reasons for the elderly to consult their GP. Syncope affects at least 20% of the population at some time and accounts for about 6% of general medical
Inappropriate vasodilatation • Neurocardiogenic syncope (e.g. vasovagal syncope, micturition syncope) • Carotid sinus hypersensitivity • Drugs (esp. anti-anginal, antihypertensive) • Orthostatic hypotension (e.g. diabetes, Parkinson’s, elderly)
Neil R Grubb MRCP is Consultant Cardiologist at Edinburgh Royal Infirmary, Edinburgh, UK. He qualified from the University of Edinburgh. His clinical interest is cardiac electrophysiology. His research interests include cardiac arrest in the community and resuscitation. Conflicts of interest: none declared.
Neurogenic • Epilepsy (including temporal lobe epilepsy – associated with bradycardia) • Vertebrobasilar ischaemia
Nicholas A Boon FRCP FESC is Consultant Cardiologist at Edinburgh Royal Infirmary, Edinburgh, UK and Honorary Reader at Edinburgh University. He qualified from the University of Cambridge and the Middlesex Hospital, London, and completed specialist training in Cambridge and Oxford. His main research interest is heart muscle disease. Conflicts of interest: none declared.
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Metabolic • Systemic hypoxia (e.g. recurrent pulmonary embolism) • Hypoglycaemia (especially in treated diabetes) Table 1
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• cough or micturition (abnormal vasomotor reflex) • neck extension (vertebrobasilar insufficiency).
This group includes situational syncope, the simple faint and vasovagal syndrome, and has a good prognosis. • Neurogenic blackouts encompass syncope due to cerebrovascular disease (e.g. brain stem ischaemia leading to drop attacks), and epilepsy. • Syncope rarely occurs because of metabolic disturbances (e.g. hypoglycaemia in insulin-treated diabetic patients). Occasionally, syncope is multifactorial, particularly in the elderly (e.g. excessive diuretic use and ventricular impairment). In the Framingham community study, although the diagnosis was not established in one-third of patients, less than 10% of syncope was thought to be cardiac. This subgroup had a particularly poor prognosis with a 5-year mortality of approximately 50% and a high incidence of sudden death. In contrast, the longterm prognosis of patients with vasovagal syncope did not differ from that of the general population.2
Syncopal episodes are more likely to be cardiac in origin when the witness describes draining of colour from the patient’s face, unconsciousness lasting less than 1 minute and a rapid recovery without confusion. Prolonged syncope, motor seizure activity, tongue biting, urinary incontinence and post-syncopal confusion and headache suggest epilepsy or a neurogenic cause. However, it is important to recognize that seizures can be triggered by cerebral hypoxia during cardiac arrhythmia. Some seizures, particularly temporal lobe epilepsy, can provoke arrhythmias. Recovery is usually rapid in cardiac syncope. Patients with vasovagal syncope may feel nauseated and unwell for several minutes after the attack. Protracted recovery (>5 minutes), depressed consciousness, headache and focal neurological symptoms suggest neurogenic syncope.
Recurrent dizziness
Family history – familial conditions such as the long QT syndrome and Brugada syndrome may cause syncope (often misdiagnosed as epilepsy) in patients with a structurally normal heart and can usually be identified by a simple 12-lead ECG. The vasovagal syndrome may also be familial.
In the evaluation of recurrent dizziness, it is important to distinguish light-headedness from rotational vertigo. The latter may be termed ‘dizziness’ by some patients, but implies a labyrinthine or middle-ear pathology. Recurrent light-headedness shares some of the mechanisms described above and can be caused by structural heart disease, conducting system disease, inappropriate vasodilatation or metabolic disturbance. In addition to these, other pathologies such as anaemia and carotid and vertebrobasilar disease should be considered. This contribution focuses on the cardiovascular causes of syncope.
Examination The pulse rhythm and rate should be examined for evidence of arrhythmia. Erect and supine blood pressure measurements are helpful; orthostatic hypotension is defined as a postural decrease in systolic blood pressure of more than 20 mmHg. However, the absence of postural hypotension on examination does not exclude intermittent orthostatic hypotension, which is affected by diurnal and environmental factors. Precordial examination may reveal evidence of structural heart disease, particularly valvular heart disease. Other important physical signs are clinical anaemia, carotid bruits and focal neurological abnormalities.
Clinical assessment Evaluation of patients with dizziness or syncope is critically dependent on careful history-taking and clinical examination – in most patients, a diagnosis can be established without complicated and expensive investigations. History The main aims of history-taking are to establish a clear description of the attack and to detect any precipitants or pattern of the symptom complex. Thus, it may be helpful to encourage patients or their carers to keep a diary of the symptoms to determine whether there is a diurnal pattern and whether symptoms are related to medication, physical activity or meal times. An accurate description of the episode from both the patient and a witness is invaluable in discriminating between neurogenic and cardiac syncope. The drug history may reveal medications that cause or contribute to symptoms by causing hypotension (particularly diuretics and vasodilators) or arrhythmia.
Investigations The history and physical examination should determine the need for subsequent investigations (Figure 1). Clinical assessment may be diagnostic, or may strongly suggest the likely diagnosis (e.g. severe aortic stenosis). If the diagnosis is unclear at this stage, it is wise to establish the presence or absence of structural heart disease, because this has important prognostic implications and suggests the likely diagnosis. The resting ECG is abnormal in about 50% of patients with syncope. Evidence of previous myocardial infarction, left ventricular (LV) hypertrophy and conducting system disease should be sought.
Premonitory symptoms of palpitation, chest discomfort and dyspnoea suggest a cardiovascular cause. Headache, confusion, hyperexcitability, olfactory hallucination and the presence of an ‘aura’ suggest a neurogenic cause. Precipitants should be identified if possible. These may include: • exertion – limited cardiac output response (aortic stenosis, hypertrophic obstructive cardiomyopathy) or exercise-induced cardiac arrhythmia • standing (orthostatic hypotension or vasovagal syncope)
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Exercise ECG: in patients with exertional symptoms, exercise ECG may reveal myocardial ischaemia, hypotension or arrhythmia. Echocardiography should be performed before exercise when there is clinical suspicion of aortic stenosis or LV outflow obstruction. Ambulatory ECG: continuous ambulatory ECG recording is useful when a cardiac cause of dizziness or syncope is suspected. 118
© 2008 Published by Elsevier Ltd.
Acute care
Investigations in syncope Obtain history from patient and witness Physical examination
Do the findings suggest a cardiac diagnosis?
Yes Consider: • Ambulatory ECG • Implantable loop recorder • Echocardiography • Electrophysiological study
No Do the findings suggest a neurological diagnosis?
Yes Consider: • EEG • Carotid Doppler • CT/MRI
Figure 2 Implantable loop recorder. These devices record ECG data and store them in memory. Patients can activate the recorder using a magnet to freeze the device’s memory.
atrioventricular (AV) block may occur, particularly at night. Other common findings are short bursts of atrial fibrillation of less than five beats, nocturnal sinus bradycardia or junctional bradycardia, and sinus arrhythmia. Episodes of Mobitz type I second-degree AV block or sinus pauses of up to 2 seconds can occur in young individuals with high vagal tone; however, sinus pauses associated with dizziness or syncope should be regarded as pathological. Abnormalities such as sinus pauses and episodes of atrial fibrillation are commonly found during recordings in elderly individuals, but these should not be assumed to be the cause of the patient’s symptoms unless the patient is symptomatic during the recording. Ambulatory ECG can identify many types of intermittent arrhythmia that cause dizziness or syncope (Figure 3), and ECG changes of myocardial ischaemia (ST segment depression or Twave inversion) may also be detected. When myocardial ischaemia is suspected as the cause of symptoms, it is vital to achieve a noise-free recording and to assess the effect of postural and respiratory changes, to avoid artefactual ST segment shift.
No Consider: • Tilt test • ECG with carotid sinus massage
Figure 1
Modern ambulatory ECG monitors can record several days of ECG information and can record at least two channels simultaneously, with timing markers and patient-activated event markers; with some devices it is also possible to record simultaneous blood pressure. Most recorders use digital memory to store ECG data.3 Interpretation of recordings requires high-speed automated analysis, verified by a technician or physician. To maximize diagnostic sensitivity, it is vital to prepare electrode sites meticulously, to ensure that electrodes are not positioned over large muscle groups and that the P-waves are visible on the ECG tracing. In many individuals with episodic dizziness or syncope, symptoms are infrequent and repeated recordings or a patientactivated ECG recorder may be required to diagnose the rhythm during symptoms. Implantable ECG recorder – in patients with infrequent symptoms, or with sudden syncope, an implantable loop recorder (Figure 2) can be used to capture the ECG during episodes. It can be programmed to automatically record abnormally rapid or slow rhythms, and in addition the patient can activate the recorder with an external remote control when symptoms occur. ECG data can be uploaded in the clinic using a pacemaker programmer. These devices are implanted using local anaesthetic, through a small infraclavicular incision, and second-generation devices will function for around 2 years. It is essential to correlate rhythm abnormality with symptoms. Disturbances of rhythm are common in ambulatory ECG recordings in healthy, asymptomatic individuals and do not necessarily represent important underlying pathology. Isolated supraventricular and ventricular extrasystoles are common and usually benign. In individuals with high vagal tone, Wenckebach second-degree
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Echocardiography is invaluable in the assessment of structural heart disease such as aortic stenosis, hypertrophic cardiomyopathy and LV impairment. Detection of regional abnormalities in LV function suggests underlying ischaemic heart disease. Tilt testing (Figure 4) is used in the diagnosis of vasovagal syndrome. There are many tilt testing protocols, but typically baseline blood pressure and heart rate recordings are obtained with the patient lying supine for 30 minutes before the table is tilted to an angle of 60° for up to 45 minutes or until symptoms are reproduced. Carotid sinus massage, intravenous isoprenaline or sublingual glyceryl trinitrate, are sometimes administered to increase the sensitivity of the test but may lead to false-positive results. Reproducibility of results within individual patients is poor and occasionally repeat testing is required. Electrophysiological (EP) study: with the development of long-duration ambulatory ECG recorders and implantable loop recorders, an invasive EP study is rarely used nowadays in the evaluation of syncope. Its main role is in the evaluation of patients with coronary heart disease and suspected ventricular 119
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Acute care
Ambulatory ECGs a Sinus rhythm followed by atrial fibrillation, rate 120 beats/minute
b Atrial fibrillation with pause of 3.6 seconds
c Atrial fibrillation with rapid ventricular response (150 beats/minute) and profound ST segment depression
d Atrial fibrillation with episode of non-sustained ventricular tachycardia, rate 210 beats/minute
e Sinus rhythm with Wenckebach second-degree atrioventricular block
Figure 3
• Third-degree AV block is characterized by complete failure of conduction between atria and ventricles with dissociation of Pwaves and QRS complexes. It is associated with a significant risk of asystole and syncope or cardiac arrest. In the absence of a reversible cause symptomatic second-degree or third-degree AV block should be treated using a permanent pacemaker, because this improves symptoms and prognosis.
tachycardia, who are being considered for defibrillator implantation. An EP study involves percutaneous placement of catheter electrodes into the heart, and assessment of the cardiac rhythm in response to provocative pacing manoeuvres and drugs.
Causes and treatments Bradycardia Bradycardia can occur because of sinus node or AV node dysfunction. Drugs that affect cardiac conduction (e.g. digoxin, βblockers, verapamil, diltiazem, and other anti-arrhythmics) are potentially reversible causes of bradycardia. The diagnosis is made by ECG or ambulatory monitoring (Figure 3). It is important to document symptoms in association with the bradycardia.
Tachycardia Ventricular tachycardia often causes syncope (particularly in patients with valve disease or ventricular dysfunction), which may be preceded by dizziness and palpitation. Atrial fibrillation and supraventricular tachycardia seldom cause syncope but may cause dizziness, particularly in the elderly and in patients with impaired cardiac function. Treatment depends on the type of tachycardia. Patients with malignant ventricular arrhymthmias (ventricular tachycardia and ventricular fibrillation) are often treated with an implantable cardioverter defibrillator and antiarrhythmic drugs.
Sinoatrial disease (sick sinus syndrome) is characterized by episodes of sinus bradycardia, sinus pauses, junctional escape rhythm and episodes of atrial fibrillation. Permanent pacing is indicated for symptomatic bradycardia or pauses, though generally pacing is not required if the pauses are shorter than 3 seconds.
Vasovagal syndrome Vasovagal syndrome is usually a reflex response to a reduction in venous return, which can occur following prolonged standing, exposure to excessive heat or a large meal. Sympathetic activation leads to vigorous contraction of the relatively underfilled ventricles and engages the reflex through stimulation of ventricular mechanoreceptors; this leads to parasympathetic activation and sympathetic withdrawal, causing vasodilatation, bradycardia or both. The diagnosis is made on tilt testing. Simple lifestyle measures are often effective remedies. These include insuring an adequate fluid and salt intake and avoiding circumstances that have triggered symptoms in the past. Patients should be advised to lie or sit down if they experience warning
AV block is caused by failure or delay of conduction between atria and ventricles. • First-degree AV block (PR interval >0.2 seconds) does not cause a change in ventricular rate and is not in itself a cause of dizziness or syncope. • Second-degree AV block is associated with failure of some atrial impulses to reach the ventricles. In Mobitz type I (Wenckebach) block, the PR interval of successive cycles increases until an atrial impulse fails to conduct to the ventricles and a pause occurs. In Mobitz type II block, conduction from atria to ventricles fails periodically, resulting in a pause, but the PR interval remains constant. Dizziness sometimes results.
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Bezold–Jarisch reflex Afferent Brain stem
Efferent Brain stem Vagal stimulation
Non-medullated vagal C- fibres
a
b
Empty ventricle High catecholamines
Sympathetic withdrawal
Bradycardia Vasodilatation
14 seconds of sinus arrest after 8 minutes of 60˚ head-up tilt testing
c
Head-up tilt testing. a The patient is positioned at 60–75% upright tilt and ECG and blood pressure are monitored. b Venous pooling reduces venous return and initially leads to increased cardiac sympathetic activity. In the afferent limb of the reflex (left), mechanoreceptor stimulation occurs via vagal C-fibres in response to vigorous contraction of underfilled ventricles. This mediates a profound efferent vagal response with withdrawal of sympathetic stimulation (right), leading to bradycardia and vasodilatation. c Positive cardio-inhibitory response to tilting. Simultaneous ECG (upper tracing) and systole blood pressure record (lower tracing) are shown.
Figure 4
beta- blockers and pacemakers) have produced inconsistent results. First-line therapy usually involves salt-loading, fludrocortisone, or beta-blockade. Midodrine (an alpha-adrenoceptor agonist) is also effective and may supplant these treatments as first-line drug therapy.4
symptoms; leg crossing can sometimes abort an attack by increasing venous return. A wide range of treatments can be tried in patients with refractory symptoms (Table 2). Responses are highly variable among patients and clinical trials (particularly those evaluating
Postural hypotension and situational syncope Postural hypotension is caused by failure of normal postural compensatory mechanisms. Hypovolaemia (haemorrhage, dehydration, excessive diuretic use), sympathetic degeneration (diabetes, Parkinson’s disease, age) and drug therapy (particularly anti-anginals, antidepressants and neuroleptic medication) can cause or aggravate the condition. Treatment is often ineffective. Patients should be advised to avoid prolonged standing and to get up slowly. Graduated elastic stockings, which reduce venous pooling, and fludrocortisone, which expands blood volume, are occasionally effective.
Drugs and devices used in the treatment of vasovagal syncope • Slow sodium* (or other salt supplements) • Fludrocortisone • Midodrine* • Disopyramide • Beta-blockers* • Selective serotonin reuptake inhibitors* (e.g. paroxetine) • Tilt training (repeated exposure helps adaptation) • Cardiac pacing* (DDI or DDD mode with rate drop algorithm)
Situational syncope is characterized by parasympathetic activation in the presence of an identifiable trigger (e.g. micturition syncope, cough syncope, vasovagal syncope in response to emotion or a noxious stimulus).
*Supported by at least one good randomized controlled trial.
Table 2
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Positive cardio-inhibitory response to carotid sinus massage
The ECG shows an 8-second period of asystole. The baseline artefact is caused by a brief convulsion. Figure 5
ischaemia with pre-existing ventricular impairment, can produce symptoms by reducing cardiac output. Ischaemia can also induce arrhythmias that themselves cause symptoms. Patients who take sublingual glyceryl trinitrate may experience dizziness or syncope as a result of vasodilatation, if they have coexisting ventricular impairment or valve disease. ◆
Carotid sinus hypersensitivity Hypersensitivity of carotid artery baroreceptors can result in parasympathetic activation with bradycardia and/or vasodilatation. In carotid sinus hypersensitivity, patients may describe dizziness or syncope when pressure is applied to the neck (e.g. when wearing a tight collar). Carotid sinus hypersensitivity may be diagnosed if 5 seconds of carotid sinus massage precipitates a fall of more than 50 mm Hg in systolic blood pressure or a ventricular pause of more than 3 seconds (Figure 5). Carotid sinus massage should not be attempted in patients with suspected or known carotid vascular disease (auscultate first) and simultaneous bilateral carotid massage should never be attempted. A positive response to carotid sinus massage is found in about 10% of the general elderly population, but fewer than 25% of these individuals suffer spontaneous syncope. A patient’s symptoms can therefore be unequivocally attributed to carotid sinus hypersensitivity only if they are reproduced by carotid sinus massage. The definitive treatment is permanent dual-chamber pacing.
References 1 Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. Br Med J 2004; 329: 336–41. 2 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347: 878–85. 3 Rao A, Lomax S, Ramsdale K, Ramsdale D. Ambulatory cardiac rhythm monitoring. Br J Hosp Med 2007; 68: 132–8. 4 Grubb BP. Neurocardiogenic syncope. N Engl J Med 2005; 352: 1004–10.
Questions
LV outflow obstruction Advanced aortic stenosis may cause exertional dizziness or syncope because of limitation of cardiac output (and sometimes ventricular arrhythmia). These symptoms signify the need for urgent assessment with a view to aortic valve replacement. Hypertrophic obstructive cardiomyopathy is associated with restricted cardiac output during stress (e.g. exercise, emotion, fever). Diagnosis of both conditions is with echocardiography. Hypertrophic obstructive cardiomyopathy is treated with negatively inotropic drugs (e.g. β-blockers, verapamil), which reduce the outflow tract gradient and paradoxically improve cardiac output. Percutaneous catheter delivered alcohol septal ablation or surgery (myectomy) are used in more advanced cases. Myocardial ischaemia can produce dizziness or syncope via several distinct mechanisms. Severe global ischaemia, or regional
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• What drugs may be used to treat vasovagal syncope, and why? • When is a single as opposed to a dual chamber pacemaker indicated in a case of heart block? • Name 3 types of heart block and 2 other arrhythmias that may cause syncope. • Consider the strengths and pitfalls of 6 investigations commonly carried out in a case of unexplained syncope. • Draw up a table which could be used to aid diagnosis of syncope in the Emergency Department. Use 3 columns, headed ‘vasovagal’, ‘arrhythmia’, and ‘epilepsy’, and complete rows titled ‘past history’, ‘prodrome’, ‘features of the attack’, and ‘recovery’.
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Practice points
not necessarily establish the cause of that patient’s symptoms • Ambulatory ECG monitoring is most useful when the patient experiences symptoms during the recording period • Head-up tilt testing is likely to reveal the cause of syncope in patients who do not have serious heart disease • LV function is a key determinant of prognosis in patients with cardiac syncope
• In many cases, a diagnosis of syncope can be made on the history and examination alone • The pattern and description of episodes indicates the likely type of syncope and should determine subsequent investigation • Discovery of common pathology in an elderly patient (e.g. osteoarthritis of the neck, sinus node disease) does
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Dizzy spells and syncope: investigation and management
Relevance to the curriculum 1.0 Good clinical care 1.1 History, examination, diagnosis, record keeping, safe prescribing and reflective practice 7.0 Recognition and management of the acutely ill 7.1 Core skills in relation to acute illness
Neil R Grubb Nicholas A Boon
admissions in the UK.1 Recurrent symptoms are particularly disabling because they affect an individual’s ability to work and to drive, increase susceptibility to falls and associated injuries, and reduce independence in the elderly.
Abstract Dizziness and syncope are common symptoms in the general population, especially the elderly. Syncope can be disabling and result in physical injury and loss of independance. Causes can be divided into arrhythmia, mechanical reduction in cardiac output, inappropriate vasodilatation, neurogenic and metabolic. Patients with cardiac syncope have a poor prognosis unless the cause is quickly identified and treated. The key to making a diagnosis is obtaining a clear history from the patient or a witness of the temporal pattern of symptoms including precipitants, a description of the blackout itself, and speed of recovery. Examination focuses on identification of signs of structural heart disease and postural hypotension. If the history suggests a cardiac diagnosis, echocardiography and ambulatory ECG recording are helpful investigations. For patients with intermittent symptoms suggesting arrhythmia, implantable ECG loop recorders are increasingly used. Tilt testing is used to investigate possible vasovagal syncope, and EEG or MRI head scan can be used to identify potential neurologocal causes of blackouts. Cardiovascular causes of syncope are treated by removal of reversible triggers (e.g. drugs that cause bradycardia or hypotension) or by treatment of the underlying condition (e.g. permanent pacemaker for symptomatic bradycardia, aortic valve surgery for aortic stenosis). Vasovagal syncope is more difficult to treat but can be helped by avoiding identifiable triggers, use of medication and in some cases dual chamber pacing.
Recurrent syncope Syncope is defined as a blackout caused by reduced cerebral perfusion, but can be difficult to distinguish from other causes of loss of consciousness. Recurrent blackouts have four principal mechanisms (Table 1). • Cardiac syncope occurs in patients with structural heart disease or conducting system disease, and also results from a decrease in cardiac output caused by cardiac arrhythmia, valve disease (e.g. aortic stenosis), ventricular impairment or another mechanical problem. Patients with recurrent syncope who have structural heart disease have a poorer diagnosis than any other group. • Inappropriate vasodilatation is the most common cause of recurrent syncope in patients with a structurally normal heart.
Causes of recurrent syncope Arrhythmia • Bradycardia (e.g. sinus node disease, atrioventricular block) • Tachycardia (particularly ventricular tachycardia) Mechanical causes of reduced cardiac output • Extensive myocardial ischaemia/LV dysfunction • Ventricular outflow obstruction (e.g. aortic stenosis, hypertrophic obstructive cardiomyopathy) • Pulmonary embolism • Cough syncope
Keywords arrhythmia; dizziness; ECG/ambulatory ECG; elderly; hypotension; pacemaker; syncope; tilt testing
Dizziness affects about one-third of individuals over the age of 65 years, and is one of the most common reasons for the elderly to consult their GP. Syncope affects at least 20% of the population at some time and accounts for about 6% of general medical
Inappropriate vasodilatation • Neurocardiogenic syncope (e.g. vasovagal syncope, micturition syncope) • Carotid sinus hypersensitivity • Drugs (esp. anti-anginal, antihypertensive) • Orthostatic hypotension (e.g. diabetes, Parkinson’s, elderly)
Neil R Grubb MRCP is Consultant Cardiologist at Edinburgh Royal Infirmary, Edinburgh, UK. He qualified from the University of Edinburgh. His clinical interest is cardiac electrophysiology. His research interests include cardiac arrest in the community and resuscitation. Conflicts of interest: none declared.
Neurogenic • Epilepsy (including temporal lobe epilepsy – associated with bradycardia) • Vertebrobasilar ischaemia
Nicholas A Boon FRCP FESC is Consultant Cardiologist at Edinburgh Royal Infirmary, Edinburgh, UK and Honorary Reader at Edinburgh University. He qualified from the University of Cambridge and the Middlesex Hospital, London, and completed specialist training in Cambridge and Oxford. His main research interest is heart muscle disease. Conflicts of interest: none declared.
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Metabolic • Systemic hypoxia (e.g. recurrent pulmonary embolism) • Hypoglycaemia (especially in treated diabetes) Table 1
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• cough or micturition (abnormal vasomotor reflex) • neck extension (vertebrobasilar insufficiency).
This group includes situational syncope, the simple faint and vasovagal syndrome, and has a good prognosis. • Neurogenic blackouts encompass syncope due to cerebrovascular disease (e.g. brain stem ischaemia leading to drop attacks), and epilepsy. • Syncope rarely occurs because of metabolic disturbances (e.g. hypoglycaemia in insulin-treated diabetic patients). Occasionally, syncope is multifactorial, particularly in the elderly (e.g. excessive diuretic use and ventricular impairment). In the Framingham community study, although the diagnosis was not established in one-third of patients, less than 10% of syncope was thought to be cardiac. This subgroup had a particularly poor prognosis with a 5-year mortality of approximately 50% and a high incidence of sudden death. In contrast, the longterm prognosis of patients with vasovagal syncope did not differ from that of the general population.2
Syncopal episodes are more likely to be cardiac in origin when the witness describes draining of colour from the patient’s face, unconsciousness lasting less than 1 minute and a rapid recovery without confusion. Prolonged syncope, motor seizure activity, tongue biting, urinary incontinence and post-syncopal confusion and headache suggest epilepsy or a neurogenic cause. However, it is important to recognize that seizures can be triggered by cerebral hypoxia during cardiac arrhythmia. Some seizures, particularly temporal lobe epilepsy, can provoke arrhythmias. Recovery is usually rapid in cardiac syncope. Patients with vasovagal syncope may feel nauseated and unwell for several minutes after the attack. Protracted recovery (>5 minutes), depressed consciousness, headache and focal neurological symptoms suggest neurogenic syncope.
Recurrent dizziness
Family history – familial conditions such as the long QT syndrome and Brugada syndrome may cause syncope (often misdiagnosed as epilepsy) in patients with a structurally normal heart and can usually be identified by a simple 12-lead ECG. The vasovagal syndrome may also be familial.
In the evaluation of recurrent dizziness, it is important to distinguish light-headedness from rotational vertigo. The latter may be termed ‘dizziness’ by some patients, but implies a labyrinthine or middle-ear pathology. Recurrent light-headedness shares some of the mechanisms described above and can be caused by structural heart disease, conducting system disease, inappropriate vasodilatation or metabolic disturbance. In addition to these, other pathologies such as anaemia and carotid and vertebrobasilar disease should be considered. This contribution focuses on the cardiovascular causes of syncope.
Examination The pulse rhythm and rate should be examined for evidence of arrhythmia. Erect and supine blood pressure measurements are helpful; orthostatic hypotension is defined as a postural decrease in systolic blood pressure of more than 20 mmHg. However, the absence of postural hypotension on examination does not exclude intermittent orthostatic hypotension, which is affected by diurnal and environmental factors. Precordial examination may reveal evidence of structural heart disease, particularly valvular heart disease. Other important physical signs are clinical anaemia, carotid bruits and focal neurological abnormalities.
Clinical assessment Evaluation of patients with dizziness or syncope is critically dependent on careful history-taking and clinical examination – in most patients, a diagnosis can be established without complicated and expensive investigations. History The main aims of history-taking are to establish a clear description of the attack and to detect any precipitants or pattern of the symptom complex. Thus, it may be helpful to encourage patients or their carers to keep a diary of the symptoms to determine whether there is a diurnal pattern and whether symptoms are related to medication, physical activity or meal times. An accurate description of the episode from both the patient and a witness is invaluable in discriminating between neurogenic and cardiac syncope. The drug history may reveal medications that cause or contribute to symptoms by causing hypotension (particularly diuretics and vasodilators) or arrhythmia.
Investigations The history and physical examination should determine the need for subsequent investigations (Figure 1). Clinical assessment may be diagnostic, or may strongly suggest the likely diagnosis (e.g. severe aortic stenosis). If the diagnosis is unclear at this stage, it is wise to establish the presence or absence of structural heart disease, because this has important prognostic implications and suggests the likely diagnosis. The resting ECG is abnormal in about 50% of patients with syncope. Evidence of previous myocardial infarction, left ventricular (LV) hypertrophy and conducting system disease should be sought.
Premonitory symptoms of palpitation, chest discomfort and dyspnoea suggest a cardiovascular cause. Headache, confusion, hyperexcitability, olfactory hallucination and the presence of an ‘aura’ suggest a neurogenic cause. Precipitants should be identified if possible. These may include: • exertion – limited cardiac output response (aortic stenosis, hypertrophic obstructive cardiomyopathy) or exercise-induced cardiac arrhythmia • standing (orthostatic hypotension or vasovagal syncope)
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Exercise ECG: in patients with exertional symptoms, exercise ECG may reveal myocardial ischaemia, hypotension or arrhythmia. Echocardiography should be performed before exercise when there is clinical suspicion of aortic stenosis or LV outflow obstruction. Ambulatory ECG: continuous ambulatory ECG recording is useful when a cardiac cause of dizziness or syncope is suspected. 118
© 2008 Published by Elsevier Ltd.
Acute care
Investigations in syncope Obtain history from patient and witness Physical examination
Do the findings suggest a cardiac diagnosis?
Yes Consider: • Ambulatory ECG • Implantable loop recorder • Echocardiography • Electrophysiological study
No Do the findings suggest a neurological diagnosis?
Yes Consider: • EEG • Carotid Doppler • CT/MRI
Figure 2 Implantable loop recorder. These devices record ECG data and store them in memory. Patients can activate the recorder using a magnet to freeze the device’s memory.
atrioventricular (AV) block may occur, particularly at night. Other common findings are short bursts of atrial fibrillation of less than five beats, nocturnal sinus bradycardia or junctional bradycardia, and sinus arrhythmia. Episodes of Mobitz type I second-degree AV block or sinus pauses of up to 2 seconds can occur in young individuals with high vagal tone; however, sinus pauses associated with dizziness or syncope should be regarded as pathological. Abnormalities such as sinus pauses and episodes of atrial fibrillation are commonly found during recordings in elderly individuals, but these should not be assumed to be the cause of the patient’s symptoms unless the patient is symptomatic during the recording. Ambulatory ECG can identify many types of intermittent arrhythmia that cause dizziness or syncope (Figure 3), and ECG changes of myocardial ischaemia (ST segment depression or Twave inversion) may also be detected. When myocardial ischaemia is suspected as the cause of symptoms, it is vital to achieve a noise-free recording and to assess the effect of postural and respiratory changes, to avoid artefactual ST segment shift.
No Consider: • Tilt test • ECG with carotid sinus massage
Figure 1
Modern ambulatory ECG monitors can record several days of ECG information and can record at least two channels simultaneously, with timing markers and patient-activated event markers; with some devices it is also possible to record simultaneous blood pressure. Most recorders use digital memory to store ECG data.3 Interpretation of recordings requires high-speed automated analysis, verified by a technician or physician. To maximize diagnostic sensitivity, it is vital to prepare electrode sites meticulously, to ensure that electrodes are not positioned over large muscle groups and that the P-waves are visible on the ECG tracing. In many individuals with episodic dizziness or syncope, symptoms are infrequent and repeated recordings or a patientactivated ECG recorder may be required to diagnose the rhythm during symptoms. Implantable ECG recorder – in patients with infrequent symptoms, or with sudden syncope, an implantable loop recorder (Figure 2) can be used to capture the ECG during episodes. It can be programmed to automatically record abnormally rapid or slow rhythms, and in addition the patient can activate the recorder with an external remote control when symptoms occur. ECG data can be uploaded in the clinic using a pacemaker programmer. These devices are implanted using local anaesthetic, through a small infraclavicular incision, and second-generation devices will function for around 2 years. It is essential to correlate rhythm abnormality with symptoms. Disturbances of rhythm are common in ambulatory ECG recordings in healthy, asymptomatic individuals and do not necessarily represent important underlying pathology. Isolated supraventricular and ventricular extrasystoles are common and usually benign. In individuals with high vagal tone, Wenckebach second-degree
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Echocardiography is invaluable in the assessment of structural heart disease such as aortic stenosis, hypertrophic cardiomyopathy and LV impairment. Detection of regional abnormalities in LV function suggests underlying ischaemic heart disease. Tilt testing (Figure 4) is used in the diagnosis of vasovagal syndrome. There are many tilt testing protocols, but typically baseline blood pressure and heart rate recordings are obtained with the patient lying supine for 30 minutes before the table is tilted to an angle of 60° for up to 45 minutes or until symptoms are reproduced. Carotid sinus massage, intravenous isoprenaline or sublingual glyceryl trinitrate, are sometimes administered to increase the sensitivity of the test but may lead to false-positive results. Reproducibility of results within individual patients is poor and occasionally repeat testing is required. Electrophysiological (EP) study: with the development of long-duration ambulatory ECG recorders and implantable loop recorders, an invasive EP study is rarely used nowadays in the evaluation of syncope. Its main role is in the evaluation of patients with coronary heart disease and suspected ventricular 119
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Ambulatory ECGs a Sinus rhythm followed by atrial fibrillation, rate 120 beats/minute
b Atrial fibrillation with pause of 3.6 seconds
c Atrial fibrillation with rapid ventricular response (150 beats/minute) and profound ST segment depression
d Atrial fibrillation with episode of non-sustained ventricular tachycardia, rate 210 beats/minute
e Sinus rhythm with Wenckebach second-degree atrioventricular block
Figure 3
• Third-degree AV block is characterized by complete failure of conduction between atria and ventricles with dissociation of Pwaves and QRS complexes. It is associated with a significant risk of asystole and syncope or cardiac arrest. In the absence of a reversible cause symptomatic second-degree or third-degree AV block should be treated using a permanent pacemaker, because this improves symptoms and prognosis.
tachycardia, who are being considered for defibrillator implantation. An EP study involves percutaneous placement of catheter electrodes into the heart, and assessment of the cardiac rhythm in response to provocative pacing manoeuvres and drugs.
Causes and treatments Bradycardia Bradycardia can occur because of sinus node or AV node dysfunction. Drugs that affect cardiac conduction (e.g. digoxin, βblockers, verapamil, diltiazem, and other anti-arrhythmics) are potentially reversible causes of bradycardia. The diagnosis is made by ECG or ambulatory monitoring (Figure 3). It is important to document symptoms in association with the bradycardia.
Tachycardia Ventricular tachycardia often causes syncope (particularly in patients with valve disease or ventricular dysfunction), which may be preceded by dizziness and palpitation. Atrial fibrillation and supraventricular tachycardia seldom cause syncope but may cause dizziness, particularly in the elderly and in patients with impaired cardiac function. Treatment depends on the type of tachycardia. Patients with malignant ventricular arrhymthmias (ventricular tachycardia and ventricular fibrillation) are often treated with an implantable cardioverter defibrillator and antiarrhythmic drugs.
Sinoatrial disease (sick sinus syndrome) is characterized by episodes of sinus bradycardia, sinus pauses, junctional escape rhythm and episodes of atrial fibrillation. Permanent pacing is indicated for symptomatic bradycardia or pauses, though generally pacing is not required if the pauses are shorter than 3 seconds.
Vasovagal syndrome Vasovagal syndrome is usually a reflex response to a reduction in venous return, which can occur following prolonged standing, exposure to excessive heat or a large meal. Sympathetic activation leads to vigorous contraction of the relatively underfilled ventricles and engages the reflex through stimulation of ventricular mechanoreceptors; this leads to parasympathetic activation and sympathetic withdrawal, causing vasodilatation, bradycardia or both. The diagnosis is made on tilt testing. Simple lifestyle measures are often effective remedies. These include insuring an adequate fluid and salt intake and avoiding circumstances that have triggered symptoms in the past. Patients should be advised to lie or sit down if they experience warning
AV block is caused by failure or delay of conduction between atria and ventricles. • First-degree AV block (PR interval >0.2 seconds) does not cause a change in ventricular rate and is not in itself a cause of dizziness or syncope. • Second-degree AV block is associated with failure of some atrial impulses to reach the ventricles. In Mobitz type I (Wenckebach) block, the PR interval of successive cycles increases until an atrial impulse fails to conduct to the ventricles and a pause occurs. In Mobitz type II block, conduction from atria to ventricles fails periodically, resulting in a pause, but the PR interval remains constant. Dizziness sometimes results.
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Bezold–Jarisch reflex Afferent Brain stem
Efferent Brain stem Vagal stimulation
Non-medullated vagal C- fibres
a
b
Empty ventricle High catecholamines
Sympathetic withdrawal
Bradycardia Vasodilatation
14 seconds of sinus arrest after 8 minutes of 60˚ head-up tilt testing
c
Head-up tilt testing. a The patient is positioned at 60–75% upright tilt and ECG and blood pressure are monitored. b Venous pooling reduces venous return and initially leads to increased cardiac sympathetic activity. In the afferent limb of the reflex (left), mechanoreceptor stimulation occurs via vagal C-fibres in response to vigorous contraction of underfilled ventricles. This mediates a profound efferent vagal response with withdrawal of sympathetic stimulation (right), leading to bradycardia and vasodilatation. c Positive cardio-inhibitory response to tilting. Simultaneous ECG (upper tracing) and systole blood pressure record (lower tracing) are shown.
Figure 4
beta- blockers and pacemakers) have produced inconsistent results. First-line therapy usually involves salt-loading, fludrocortisone, or beta-blockade. Midodrine (an alpha-adrenoceptor agonist) is also effective and may supplant these treatments as first-line drug therapy.4
symptoms; leg crossing can sometimes abort an attack by increasing venous return. A wide range of treatments can be tried in patients with refractory symptoms (Table 2). Responses are highly variable among patients and clinical trials (particularly those evaluating
Postural hypotension and situational syncope Postural hypotension is caused by failure of normal postural compensatory mechanisms. Hypovolaemia (haemorrhage, dehydration, excessive diuretic use), sympathetic degeneration (diabetes, Parkinson’s disease, age) and drug therapy (particularly anti-anginals, antidepressants and neuroleptic medication) can cause or aggravate the condition. Treatment is often ineffective. Patients should be advised to avoid prolonged standing and to get up slowly. Graduated elastic stockings, which reduce venous pooling, and fludrocortisone, which expands blood volume, are occasionally effective.
Drugs and devices used in the treatment of vasovagal syncope • Slow sodium* (or other salt supplements) • Fludrocortisone • Midodrine* • Disopyramide • Beta-blockers* • Selective serotonin reuptake inhibitors* (e.g. paroxetine) • Tilt training (repeated exposure helps adaptation) • Cardiac pacing* (DDI or DDD mode with rate drop algorithm)
Situational syncope is characterized by parasympathetic activation in the presence of an identifiable trigger (e.g. micturition syncope, cough syncope, vasovagal syncope in response to emotion or a noxious stimulus).
*Supported by at least one good randomized controlled trial.
Table 2
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Positive cardio-inhibitory response to carotid sinus massage
The ECG shows an 8-second period of asystole. The baseline artefact is caused by a brief convulsion. Figure 5
ischaemia with pre-existing ventricular impairment, can produce symptoms by reducing cardiac output. Ischaemia can also induce arrhythmias that themselves cause symptoms. Patients who take sublingual glyceryl trinitrate may experience dizziness or syncope as a result of vasodilatation, if they have coexisting ventricular impairment or valve disease. ◆
Carotid sinus hypersensitivity Hypersensitivity of carotid artery baroreceptors can result in parasympathetic activation with bradycardia and/or vasodilatation. In carotid sinus hypersensitivity, patients may describe dizziness or syncope when pressure is applied to the neck (e.g. when wearing a tight collar). Carotid sinus hypersensitivity may be diagnosed if 5 seconds of carotid sinus massage precipitates a fall of more than 50 mm Hg in systolic blood pressure or a ventricular pause of more than 3 seconds (Figure 5). Carotid sinus massage should not be attempted in patients with suspected or known carotid vascular disease (auscultate first) and simultaneous bilateral carotid massage should never be attempted. A positive response to carotid sinus massage is found in about 10% of the general elderly population, but fewer than 25% of these individuals suffer spontaneous syncope. A patient’s symptoms can therefore be unequivocally attributed to carotid sinus hypersensitivity only if they are reproduced by carotid sinus massage. The definitive treatment is permanent dual-chamber pacing.
References 1 Chen-Scarabelli C, Scarabelli TM. Neurocardiogenic syncope. Br Med J 2004; 329: 336–41. 2 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med 2002; 347: 878–85. 3 Rao A, Lomax S, Ramsdale K, Ramsdale D. Ambulatory cardiac rhythm monitoring. Br J Hosp Med 2007; 68: 132–8. 4 Grubb BP. Neurocardiogenic syncope. N Engl J Med 2005; 352: 1004–10.
Questions
LV outflow obstruction Advanced aortic stenosis may cause exertional dizziness or syncope because of limitation of cardiac output (and sometimes ventricular arrhythmia). These symptoms signify the need for urgent assessment with a view to aortic valve replacement. Hypertrophic obstructive cardiomyopathy is associated with restricted cardiac output during stress (e.g. exercise, emotion, fever). Diagnosis of both conditions is with echocardiography. Hypertrophic obstructive cardiomyopathy is treated with negatively inotropic drugs (e.g. β-blockers, verapamil), which reduce the outflow tract gradient and paradoxically improve cardiac output. Percutaneous catheter delivered alcohol septal ablation or surgery (myectomy) are used in more advanced cases. Myocardial ischaemia can produce dizziness or syncope via several distinct mechanisms. Severe global ischaemia, or regional
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• What drugs may be used to treat vasovagal syncope, and why? • When is a single as opposed to a dual chamber pacemaker indicated in a case of heart block? • Name 3 types of heart block and 2 other arrhythmias that may cause syncope. • Consider the strengths and pitfalls of 6 investigations commonly carried out in a case of unexplained syncope. • Draw up a table which could be used to aid diagnosis of syncope in the Emergency Department. Use 3 columns, headed ‘vasovagal’, ‘arrhythmia’, and ‘epilepsy’, and complete rows titled ‘past history’, ‘prodrome’, ‘features of the attack’, and ‘recovery’.
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Practice points
not necessarily establish the cause of that patient’s symptoms • Ambulatory ECG monitoring is most useful when the patient experiences symptoms during the recording period • Head-up tilt testing is likely to reveal the cause of syncope in patients who do not have serious heart disease • LV function is a key determinant of prognosis in patients with cardiac syncope
• In many cases, a diagnosis of syncope can be made on the history and examination alone • The pattern and description of episodes indicates the likely type of syncope and should determine subsequent investigation • Discovery of common pathology in an elderly patient (e.g. osteoarthritis of the neck, sinus node disease) does
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