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Distinguishing syncopal from non-syncopal causes of fall in older people

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DOI: 10.1093/ageing/afl086 · Source: PubMed

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Age and Ageing 2006; 35-S2: ii46–ii50 © The Author 2006. Published by Oxford University Press on behalf of the British Geriatrics Society.
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Distinguishing syncopal from non-syncopal
causes of fall in older people
MICHELE BRIGNOLE
Arrhythmologic Centre, Ospedali del Tigullio, Lavagna, Italy
Address correspondence to: M. Brignole, Department of Cardiology, Ospedali del Tigullio, Via don Bobbio, 16033 Lavagna, Italy.
Email: mbrignole@asl4.liguria.it
Keywords: syncope, arrhythmias, cardiovascular diseases
Background
Syncope is the mechanism by which cardiovascular abnor-
malities may cause falls in older people. Syncope is a symp-
tom, defined as a transient, self-limited loss of
consciousness, usually leading to falling. The onset of syn-
cope is relatively rapid, and the subsequent recovery is
spontaneous, complete and usually prompt. The underlying
mechanism is a transient global cerebral hypoperfusion [1,
2]. Syncopal loss of consciousness invariably determines
loss of postural tone and, if it occurs in the upright position,
falling. Irrespective of the precise underlying cause of syn-
cope, a sudden cessation of cerebral blood flow for 6–8 s
and/or a decrease in systolic blood pressure to 60 mm Hg
has been shown to be sufficient to cause complete loss of
consciousness. Further, it has been estimated that as little as
a 20% drop in cerebral oxygen delivery is sufficient to cause
loss of consciousness.
Syncope is common amongst older people. In the
Framingham study [3], the 10-year cumulative incidence of
syncope was 6%. The incidence was not, however, con-
stant but increased more rapidly from the age of 70 years
upwards. The 10-year cumulative incidence of syncope
was 11% for both men and women aged 70–79 and 17%
and 19% for men and women, respectively, aged 80 or
over. The incidence of syncope in an elderly institutional-
ised population was 6% per year, with a 10-year prevalence
of 23% and a recurrence rate of 30% [4]. Age-associated
physiological changes in heart rate, blood pressure, cere-
bral blood flow, baroreflex sensitivity and intravascular
volume regulation, combined with comorbid conditions
and concurrent medications, may all contribute to the
higher incidence of syncope in the older population [5].
In terms of the immediate injurious consequences of
syncope, major morbidity such as fractures and motor vehi-
cle accidents has been reported in 6% of patients and minor
injury such as laceration and bruises in 29%. Recurrent syn-
cope is associated with fractures and soft-tissue injury in
12% of patients [6].
ii46
Distinguishing syncopal from non-syncopal
causes of fall
Syncope must be differentiated from other ‘non-syncopal’
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conditions associated with real or apparent transient loss of
consciousness. This differentiation is less difficult in the
situation where falls without loss of consciousness are the
presenting problem.
However, differentiating syncope from other causes
of falls is sometimes a difficult task especially in advanced
age, and up to one–quarter of syncopal events will present
as unexplained falls [7–9]. The following are some critical
issues that contribute to uncertainty in the diagnostic
evaluation:
• Amnesia for loss of consciousness makes the acquisition
of an accurate history difficult.
• Cognitive impairment influences the accuracy of recall
for events.
• Gait and balance instability and slow protective reflexes
are frequent in community-dwelling older people; in
these circumstances moderate haemodynamic changes
insufficient to cause syncope may result in falls.
It is important, therefore, to make every attempt to
obtain a witness account of episodes, although this is not
available in many instances.
Tables 1 and 2 provide the pathophysiological classi-
fication of the principal known causes of transient loss of
consciousness proposed by the Task Force on Syncope
of the European Society of Cardiology [1, 2]. The sub-
division of syncope is based on pathophysiology as
follows:
• ‘Neurally mediated (reflex) syncope’ refers to a reflex
response that, when triggered, gives rise to vasodilatation
and/or bradycardia, although the contribution of each of
these two factors to systemic hypotension and cerebral
hypoperfusion may differ considerably. The triggering
events may also vary considerably amongst individual
 Syncope and falls

Table 1. Causes of syncope, according to the classification of the Task Force on Syncope of the European Society of
Cardiology [1, 2]
Neurally mediated (reflex)
Vasovagal syncope (common faint)
Classical
Non-classical
Carotid sinus syncope
Situational syncope
Acute haemorrhage
Cough, sneeze
Gastrointestinal stimulation (swallow, defaecation, visceral pain)
Micturition (post-micturition)
Post-exercise
Post-prandial
Others (e.g. brass instrument playing, weightlifting)
Glossopharyngeal neuralgia
Orthostatic hypotension
Autonomic failure
Primary autonomic failure syndromes (e.g. pure autonomic failure, multiple system atrophy, Parkinson’s disease with autonomic failure)
Secondary autonomic failure syndromes (e.g. diabetic neuropathy, amyloid neuropathy)
Post-exercise
Post-prandial
Drug (and alcohol)-induced orthostatic syncope
Volume depletion
Haemorrhage, diarrhoea, Addison’s disease
Cardiac arrhythmias as primary cause

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Sinus node dysfunction (including bradycardia/tachycardia syndrome)
Atrioventricular conduction system disease
Paroxysmal supraventricular and ventricular tachycardias
Inherited syndromes (e.g. long QT syndrome, Brugada syndrome)
Implanted device (pacemaker, ICD) malfunction
Drug-induced proarrhythmias
Structural cardiac or cardiopulmonary disease
Cardiac valvular disease
Acute myocardial infarction / ischaemia
Obstructive cardiomyopathy
Atrial myxoma
Acute aortic dissection
Pericardial disease/tamponade
Pulmonary embolus / pulmonary hypertension
Cerebrovascular
Vascular steal syndromes

Table 2. Causes of non-syncopal attacks (commonly misdiagnosed as syncope) according the classification of the Task Force
on Syncope of the European Society of Cardiology [1, 2]
Disorders without any impairment of consciousness
Falls
Cataplexy
Drop attacks
Psychogenic pseudo-syncope
Transient ischaemic attacks (TIA) of carotid origin
Disorders without any impairment of consciousness
Metabolic disorders, including hypoglycaemia, hypoxia, hyperventilation with hypocapnia
Epilepsy
Intoxications
Vertebro-basilar transient ischaemic attack

patients. The ‘classical vasovagal syncope’ is mediated by
emotional or orthostatic stress and can be diagnosed by
history taking. ‘Carotid sinus syncope’ is defined as syn-
cope which, by history, seems to occur in close relation-
ship to accidental mechanical manipulation of the carotid
sinuses, and which can be reproduced by carotid sinus
massage. ‘Situational syncope’ refers to those forms of
neurally mediated syncope associated with specific sce-
narios (e.g. micturition, coughing, defaecating, etc.).
Often, however, neurally mediated reflex syncope has

ii47
M. Brignole
‘non-classical’ presentations. These forms are then diagnosed
by minor clinical criteria, exclusion of other causes for
syncope (absence of structural heart disease) and positive
response to tilt testing or carotid sinus massage. Exam-
ples of such ‘non-classical’ vasovagal syncope include
those situations where episodes occur without clear trig-
gering events or premonitory symptoms.
• Orthostatic hypotension refers to syncope in which the
upright position (most often movement from sitting or
lying to an upright position) causes arterial hypotension.
This occurs when the autonomic nervous system is inca-
pacitated and fails to respond to the challenges imposed
by the upright position. A second major cause is volume
depletion in which the autonomic nervous system is not
itself deranged but is unable to maintain blood pressure
due to decreased circulating volume. Note that vasovagal
syncope can also be provoked by standing (e.g. soldiers
fainting on parade), but this category of event is most
appropriately grouped under neurally mediated (reflex)
syncope.
• Cardiac arrhythmias may cause a decrease in cardiac out-
put of sufficient magnitude to cause syncope, which usu-
ally occurs irrespectively of any change in circulatory
demands.
• Structural heart disease may cause syncope when circula-
tory demands outweigh the impaired ability of the heart
to increase its output.
• ‘Steal’ syndromes may cause syncope when a blood ves-
sel supplying parts of both the brain and an upper limb
delivers a disproportionate component of perfusion to
the limb at the expense of the cerebral component (usu-
ally in response to increased limb activity and demand).
A range of other disorders may resemble syncope,
mainly in two different ways:
• Consciousness is truly lost, but the mechanism is some-
thing other than cerebral hypoperfusion. Examples are
epilepsy, several metabolic disorders (including hypoxia
and hypoglycaemia) and intoxications.
• Consciousness is only apparently lost. This is the case in
‘psychogenic pseudo-syncope’, cataplexy and drop
attacks. In psychogenic pseudo-syncope, patients may
pretend to be unconscious when they are not. This phe-
nomenon is often strongly suggested by a broader con-
text of factitious disorders, malingering and conversion.
Finally, some patients may voluntarily trigger true syn-
cope in themselves to attract attention, as a behavioural
abnormality, or to obtain some other advantage.
Table 2 lists the conditions most commonly misdiag-
nosed as syncope. Awareness of the range of differential
diagnosis is important because the clinician is commonly
confronted by patients with a history of sudden loss of con-
sciousness (real or apparent) that may be due to causes not
associated with decreased cerebral blood flow, for example
seizure or conversion reaction.
A major limitation of this classification is the fact that
more than one pathophysiological factor may contribute to
the symptoms. For instance, in the setting of valvular aortic
ii48
stenosis or left ventricular outflow tract obstruction,
syncope may not be the result solely of restricted cardiac
output but may be partly due to inappropriate neurally
mediated reflex vasodilation and/or primary cardiac
arrhythmia [10]. Similarly, a neural reflex component (pre-
venting or delaying vasoconstrictor compensation) appears
to play an important role when syncope occurs in associa-
tion with certain brady- and tachyarrhythmias [11, 12].
Most frequent causes of syncopal falls in
older people
The commonest causes of syncope in older adults are (i)
orthostatic hypotension, (ii) carotid sinus syndrome, (iii)
various forms of neurally mediated syncope and (iv) cardiac
arrhythmias [9].
Orthostatic hypotension
The prevalence of orthostatic hypotension varies from ≥6%
in community-dwelling older people to 33% in hospital inpa-
tients. Orthostatic hypotension is an attributable cause of
syncope in up to 30% of older patients. In symptomatic
patients, 25% have ‘age-associated’ or idiopathic orthostatic
hypotension. This occurs when in the absence of any other
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identifiable precipitating factors the autonomic nervous sys-
tem fails to respond adequately to the upright position by
vasoconstrictor mechanisms (mainly on capacitance vessels),
resulting in a reduction in blood pressure (and, hence, in cere-
bral perfusion) of sufficient magnitude to give rise to symp-
toms. In the others, orthostatic hypotension is predominantly
due to identifiable causes, such as culprit medications, prim-
ary autonomic failure, secondary autonomic failure (diabetes),
Parkinson’s disease or multisystem atrophy.
Supine systolic hypertension is often present in older
patients with orthostatic hypotension. Hypertension not
only blunts the capacity and efficiency of cerebral autoregu-
lation and increases the risk of cerebral ischaemia from sud-
den falls in blood pressure, but also complicates treatment,
given that most agents used for the treatment of orthostatic
hypotension will exacerbate supine hypertension [9, 13, 14].
Carotid sinus syndrome
Carotid sinus syndrome rarely occurs before age 40. The
prevalence increases with advancing years and with cardio-
vascular, cerebrovascular and neurodegenerative co-mor-
bidity [15]. Cardioinhibitory carotid sinus syndrome is an
attributable cause of symptoms in up to 20% of elderly
patients with syncope [9]. Further study is ongoing to assess
the true frequency more accurately, but it is a fair assump-
tion that it will prove to be more common than previously
thought. Carotid sinus syndrome is diagnosed in patients
who are found to have an abnormal response to carotid
sinus massage (carotid sinus hypersensitivity) and an other-
wise negative investigational workup for syncope. A posit-
ive response is defined as a ventricular pause ≥3 s and/or a
fall in systolic blood pressure ≥50 mm Hg which reproduces
spontaneous symptoms [15].
Carotid sinus massage is not without risk, the main com-
plication being neurological, i.e. transient cerebral ischaemia

or stroke. The reported incidence is low, ranging in three
studies from 0.17 to 0.45% [1, 2]. In individuals at high risk
of stroke due to known carotid artery disease, carotid sinus
massage should be avoided.
Neurally mediated syncope
Up to 15% of syncope is due to other forms of neurally
mediated origin [9].
‘Classical vasovagal syncope’ (mediated by emotional or
orthostatic stress) is comparatively rarely observed amongst
older people [16]. ‘Non-classical’ presentations are much
more frequent, and the diagnosis of these forms is estab-
lished by minor clinical criteria, exclusion of other causes of
syncope (absence of structural heart disease) and a positive
response to tilt testing. Examples of non-classical vasovagal
syncope include episodes without clear triggering events or
premonitory signs. In over half of these, the cause is found
to be related to prescription of cardiovascular medications.
The pattern of blood pressure and heart rate responses dur-
ing tilt testing is similar to that described in younger
patients, but the prevalence of patterns differs. Bradyar-
rhythmic responses (VASIS 2B) are less common, and pro-
gressive hypotensive responses (VASIS 3) and chronotropic
incompetence are more common, although patterns charac-
teristic of autonomic failure are more common in drug-
related episodes [17]. ‘Situational syncope’ is also frequent.
Micturition and gastrointestinal stimulation (swallowing,
defecation, visceral pain) are the most common concomi-
tants of situational syncope amongst older people.
Cardiac arrhythmias
Cardiac arrhythmias account for up to 20% of syncope
amongst older patients [9]. Arrhythmia-related syncope is
identified by one or more of the following ECG findings
[1, 2]:
• Sinus bradycardia <40 beats/min or repetitive sinoatrial
blocks or sinus pauses;
• Mobitz II second- or third-degree atrioventricular block;
• Rapid paroxysmal supraventricular tachycardia or ven-
tricular tachycardia.
In older patients referred for investigation of unex-
plained syncope, Holter monitoring rarely yields a diagnostic
symptom–ECG correlation because of the long syncope-
free intervals which usually occur. There is therefore a case
to be made for the insertion of an implantable loop recorder
to achieve a diagnosis. In a reported series using this tech-
nique, a higher diagnostic yield for causative arrhythmia was
obtained in older patients than those in younger age groups,
with a corresponding treatment success rate [18].
Risk stratification
In patients presenting with syncope, the presence of struc-
tural heart disease constitutes a major and important risk
factor for sudden death and overall mortality. When the
mechanism of syncope is not evident, the presence of sus-
pected or certain heart disease is associated with a higher
risk of arrhythmias and a higher mortality at 1 year. The
detection and diagnosis of cardiac syncope are therefore of
Syncope and falls
particular importance prognostically and to determine the
commensurate approach to management. Particularly
important indicators of possible cardiac syncope include the
following:
• Known severe structural heart disease is present;
• There are electrocardiographic abnormalities such as
bundle branch block, atrioventricular block or sinus
bradycardia;
• Syncope has occurred during exertion or in the supine
position;
• Syncope is preceded by palpitation or accompanied by
chest pain.
When cardiac syncope is suspected, full cardiac evalua-
tion is warranted.
By contrast, neurally mediated syncope and orthostatic
hypotension have a good prognosis. Syncope of unknown
cause represents a heterogeneous group at intermediate risk.
In general, in the process of risk stratification the risk of
mortality is largely a reflection of underlying co-morbidity.
Nevertheless, irrespective of this, patients with syncope
continue to be at risk of physical injury [1, 2].
Implications for treatment
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Identifying the mechanism of syncope has obvious implica-
tions for the selection of appropriate mechanism-specific
treatment. The principal goals of treatment are (i) preven-
tion of syncope recurrence and related injuries and (ii) dimi-
nution of mortality risk.
Orthostatic hypotension
Drug-induced autonomic failure is probably the most fre-
quent cause of orthostatic hypotension. The principal treat-
ment strategy is elimination of the offending agents, mainly
diuretics and vasodilators. Alcohol is also commonly associ-
ated with orthostatic intolerance [1, 2]. A number of addi-
tional treatment strategies, applied alone or as a
combination of measures, may be appropriately considered
on an individual patient basis. These include chronic expan-
sion of intravascular volume, fludrocortisone in low dose,
raising the head of the bed on blocks to permit gravitational
exposure during sleep and the use of drugs which increase
peripheral resistance (i.e. midodrine) [1, 2].
Carotid sinus syndrome
Cardiac pacing appears to be beneficial in the cardioinhibi-
tory and mixed forms of the carotid sinus syndrome.
Although comparatively few controlled trials have been
undertaken, pacing is acknowledged to be the treatment of
choice when bradycardia has been documented. Single-
chamber atrial pacing is not appropriate for vasovagal syn-
cope, and in carotid sinus syndrome, dual-chamber pacing is
generally preferred over single-chamber ventricular pacing
[1, 2].
Neurally mediated syncope
In general, education and reassurance are sufficient for most
patients. Modification or discontinuation of hypotensive
drug treatment for concomitant conditions and avoidance
ii49
M. Brignole
of triggering events in situational syncope are other first-line
measures for the prevention of syncope recurrences. Treat-
ment is not necessary for patients who have sustained a sin-
gle syncopal episode and are not experiencing syncope in
high-risk settings. Additional treatment may be necessary in
high-risk or high-frequency situations, when syncope is very
frequent, i.e. alters the quality of life or is recurrent and
unpredictable (absence of premonitory symptoms) and/or
exposes patients to high risk of trauma [1, 2].
Many drugs have been used in the treatment of vasova-
gal syncope. These have included (for example) beta-blockers,
disopyramide, scopolamine, clonidine, theophylline, fludro-
cortisone, ephedrine, etilefrine, midodrine and serotonin
reuptake inhibitors. In general, while the results have
appeared promising in uncontrolled trials or short-term
controlled trials, long-term placebo-controlled prospective
studies have failed to show benefit of the active drug over
placebo. To date, there are insufficient data to support the
use of any concomitant pharmacological therapy for vas-
ovagal syncope [1, 2].
The role of cardiac pacing for neurally mediated syncope
is not yet fully established. Randomised trials have given
controversial results. However, it is possible that cardiac
pacing may be useful when a severe bradycardia or asystole
is documented to be present at the time of spontaneous
syncope [1, 2].
Cardiac arrhythmias as primary cause
Syncope due to cardiac arrhythmias must receive treatment
appropriate to the cause in all patients in whom it is life-
threatening and when there is a high risk of injury. Cardiac
pacing, implantable cardioverter defibrillators and catheter
ablation are the usual treatments deployed, depending on
the mechanism of syncope involved [1, 2].
Key points
• Syncope is the mechanism by which cardiovascular
abnormalities may cause falls in older people.
• The commonest causes of syncope in older adults are
orthostatic hypotension, carotid sinus syndrome and
neurally mediated syncope (other than carotid sinus) and
cardiac arrhythmias.
• Differentiating syncope from other causes of falls is
sometimes a difficult task especially in the old.
• Structural heart disease is a major risk factor for sudden
death and overall mortality in patients with syncope. Car-
diovascular risk stratification is possible based on mark-
ers of co-existing cardiac disease.
• When cardiac syncope is suspected, systematic cardiac
evaluation and investigation are essential.
• Identifying the mechanism of syncope has obvious
implications for the selection of a mechanism-specific
treatment.
• The principal goals of treatment are prevention of synco-
pal recurrences and related injuries and diminution of
mortality risk.
ii50
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Conflicts of interest
No conflict to declare.
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