THEME: Fits, faints and funny tur ns

Dizziness and loss

of consciousness
Cardiovascular causes
Jeremy J Wright,
Leonard F Arnolda

BACKGROUND Dizziness and loss of consciousness are common clinical problems presenting
in general practice.
OBJECTIVE This article aims to provide the practitioner with a pragmatic and logical approach
to identifying the cardiovascular causes of dizziness and loss of consciousness.
DISCUSSION A range of disorders with varying pathology cause a transient loss of
consciousness associated with postural collapse (syncope) by interruption of blood flow to
the brain. Syncope and seizures are the only common causes of recurrent episodes of loss of
consciousness. The vasovagal reaction or ‘common faint’ and postural hypotension are both
common and benign causes of syncope. Syncope can also result from cardiac causes that Jeremy J Wright,
include disorders of cardiac rhythm and mechanical obstruction to cardiac output. Cardiac MBBS (Hons), is a
causes of syncope are associated with much higher morbidity and mortality than postural cardiology registrar,
hypotension or fainting. Specific treatment is available for the various cardiac causes of the Advanced Heart
Failure and Cardiac
syncope and thus accurate diagnosis is imperative.
Transplant Unit,
Royal Perth Hospital,
Western Australia.
Syncope
L oss of consciousness is a result of widespread
interruption of cerebral cortical or brain stem
function. Syncope, a transient loss of consciousness
The causes of syncope may be classified into three
groups by the underlying pathophysiology:
Leonard F Arnolda,
MBBS, FRACP,
PhD, is Professor
of Cardiology,
associated with postural collapse, is caused by cere- • neurally mediated reflex syncopal syndromes
Royal Perth Hospital,
bral hypoperfusion. Syncope is usually brief. If loss • orthostatic syncope, and The University of
of consciousness is prolonged other causes must be • cardiac syncope (Table 1). Western Australia,
considered including a seizure and sudden cardiac and the Western
Presyncope Australian Institute
death. Therefore, a witnessed episode lasting more for Medical Research.
than a few seconds needs the urgent institution of Syncope often has a prodrome, called presyncope.
appropriate first aid measures. The symptoms of presyncope (or faintness) include
Recurrent episodes of loss of consciousness are lightheadedness, blurred vision, sweating, tinnitus,
nearly always caused by seizures or syncope. nausea and weakness. Presyncope is more common
Distinguishing between these possibilities can be dif- than syncope and its causes can be classified in the
ficult. Features that suggest seizures include waking same way. Patients often complain of dizziness and
with a cut tongue, déjà vu or jamaís vu, an association it can be difficult to determine if they mean pre-
with emotional stress, head turning during, or confu- syncope or vertigo. This distinction is important
sion following the loss of consciousness. Features that because vertigo is caused by inner ear or brain
suggest syncope include prodromal symptoms (pre- stem disease.
syncope) and loss of consciousness associated with In reporting the frequency and prognosis of
prolonged sitting or standing.1 Myoclonic jerks may various causes of syncope we have relied heavily
be seen in syncope and misinterpreted as evidence of on a recent report from the Framingham Cohort2
a seizure, a so-called ‘convulsive syncope’. (Table 2). Because this study is community based,

Reprinted from Australian Family Physician Vol. 32, No. 4, April 2003 • 207
n Dizziness and loss of consciousness – cardiovascular causes

Table 1. Causes of syncope we believe it is more likely to reflect patients seen

in general practice than is the reported experience
Neurally mediated reflex syncopal syndromes
of a tertiary referral centre.
• Vasovagal faint (common faint)
– situational faint Neurally mediated reflex syncopal
– cough, sneeze syndromes
– gastrointestinal stimulation
There are many syndromes in this class. What they
(swallow, defaecation, visceral pain)
have in common is arterial and venous vasodilata-
– micturition (postmicturition)
tion and relative or absolute bradycardia that is
– postexercise
mediated by the inappropriate triggering of a
– others (eg. brass instrument playing,
weightlifting, postprandial) reflex autonomic response.
– glossopharyngeal and trigeminal neuralgia Vasovagal episodes
Orthostatic
• Autonomic failure
The vasovagal (common) faint is the most fre-
– primary autonomic failure syndromes
quently identified cause of syncope. 2 Noxious
(eg. pure autonomic failure, multiple system stimuli (emotional or physical) cause an increase in
atrophy, Parkinson disease with autonomic sympathetic activity. It is postulated that this
failure) increase in sympathetic activity causes cardiac
– secondary autonomic failure syndromes (eg. hypercontractility and stimulation of cardiac
diabetic neuropathy, amyloid neuropathy) stretch receptors. These receptors may act on the
– drugs and alcohol brainstem to reduce sympathetic drive and
• Volume depletion increase parasympathetic drive. The resulting
– haemorrhage, diarrhoea, Addison disease peripheral vasodilatation and relative bradycardia
Cardiac syncope causes progressive hypotension resulting in
• Arrhythmia syncope unless the cycle is interrupted.
– sinus node dysfunction (including Tilt table testing is often part of the diagnostic
bradycardia/tachycardia syndrome) pathway. The test is positive if symptoms are
– atrioventricular conduction system disease reproduced and syncope is observed. Data from
– paroxysmal supraventricular and ventricular the Framingham Study demonstrate that patients
tachycardia
with vasovagal syncope, compared to those
• Structural heart disease
without, have no increased risk of death (of any
– cardiac valvular disease
cause), myocardial infarction, or death from coro-
– acute myocardial infarction/ischaemia
nary disease.2 Initial treatment is education about
– obstructive cardiomyopathy
the process and advice to ‘go-to-ground’ when an
– atrial myxoma
impending event is recognised to reduce the risk of
– acute aortic dissection
injury. General measures include avoidance of
– pericardial disease/tamponade
dehydration, prolonged fasting, prolonged upright
– pulmonary embolus/pulmonary
posture, hot confining environments and known
hypertension
‘triggers’, eg. venepuncture. Concurrent vasodila-
tors may exacerbate vasovagal syncope.3

Table 2. Causes of first episode of syncope*

Cause of first episode of syncope Frequency % Adjusted hazard ratio for death (95% CI)
Vasovagal
Orthostatic
21
9 } 1.08 (0.88–1.34)

Cardiac 10 2.01 (1.48–2.73)

Unknown 37 1.32 (1.09–1.60)

* Data from the Framingham Heart Study that studied a general population of 7814 participants
for a mean of 17 years, demonstrated that 21.2% of first reports of syncope were vasovagal.2

208 • Reprinted from Australian Family Physician Vol. 32, No. 4, April 2003
 Dizziness and loss of consciousness – cardiovascular causes n

If more aggressive treatment is required Cardiac syncope

patients should be referred on. Further treatment Cardiac syncope is due to a sudden reduction in
may be guided by tilt table testing and implantable cardiac output. In the Framingham Heart Study
loop recording. Treatment options include ß-block- 10% of first syncopal episodes were cardiac and
ers, volume expansion, vasoconstrictors such as these patients had double the risk of death from
midodrine, tilt table training and permanent pacing. any cause.2 The most important predictor of mortal-
ity is the severity of the underlying heart disease.3
Orthostatic syncope Identification of the cause is important because
Orthostatic syncope is due to hypotension on specific therapy may be available. Cardiac syncope
assumption of upright posture and is responsible may have an arrhythmic or mechanical cause.
for 9% of first syncopal episodes.2 This may be
caused by: Rhythm disturbance
• reduced intravascular volume, or Either very slow or very fast heart rates can result
• inadequate vasoconstriction. in a marked decrease in cardiac output and reduce
It is differentiated from neurally mediated reflex cerebral perfusion. Bradyarrhythmias result from
syncope by occurring soon after a change in disorders of the sinus node and/or atrioventricular
posture and without bradycardia. It can be conduction. Syncope may be precipitated by an
demonstrated by measuring blood pressure after ischaemic event or drugs that impair conduction,
resting supine for five minutes, and then at one eg. beta blockers (including eye drops), digoxin,
and three minutes after standing. Orthostatic calcium channel blockers and anti-arrhythmic
hypotension is defined as a decrease in the sys- drugs. Treatment is withdrawal of the offending
tolic blood pressure of >Ž20 mmHg, or a reduction agent with permanent pacing often required.
of systolic blood pressure to <90 mmHg on stand- Ventricular tachycardia is a frequent and serious
ing The prognosis is generally good depending cause of syncope that may progress to sudden cardiac
upon comorbidities and the underlying cause, the death. Drug therapy alone may be sufficient,
main risk being an elderly person sustaining although some patients require an implantable pace-
an injury. maker cardioverter defibrillator (ICD).
Reduced intravascular volume is commonly Supraventricular tachyarrhythmias are an uncommon
seen in patients treated with diuretics, with poorly cause of syncope, usually at the onset or termination
controlled diabetes, following an alcoholic binge of the arrhythmia. Treatment options include drug
and acute haemorrhage. therapy and possibly radio frequency ablation.
Inadequate vasoconstriction is common in the The diagnosis of an arrhythmic cause of
elderly. It may be primary autonomic insufficiency syncope is often suggested by the baseline electro-
but is more likely to be secondary. Common sec- cardiogram (ECG) but is confirmed by symptom
ondary causes include: ECG correlation. If symptoms occur as frequently
• prolonged bed rest as once per week, a 24 hour Holter monitor may
• peripheral neuropathy (eg. diabetic, alcoholic, help in diagnosis. An external ECG event monitor
amyloid), and such as King of Hearts® can monitor for a longer
• drugs. period of time, eg. two weeks. In difficult cases an
It is easy to recognise antihypertensives and implantable loop recorder is available. These are
vasodilators but many noncardiac drugs can also small devices that are implanted subcutaneously
impair vasoconstriction, eg. amitriptyline, under local anaesthetic and last up to two years,
haloperidol, prazosin and L-dopa. In practice, thereby allowing symptom ECG correlation.
successful treatment does not hinge on identifying An invasive electrophysiology study can often
the precise mechanism. Offending agents should predict the cause of syncope and in certain circum-
be removed. Nonpharmacological measures such stances may be diagnostic. A normal study however,
as increasing salt intake or wearing compression cannot completely exclude an arrhythmic cause.
stockings should be tried. Pharmacological treat-
ments are directed at increasing vascular volume Mechanical causes
(fludrocortisone) or increasing vascular tone Mechanical causes are in general obstructive
(midodrine). lesions. It is important to identify symptomatic
Reprinted from Australian Family Physician Vol. 32, No. 4, April 2003 • 209
n Dizziness and loss of consciousness – cardiovascular causes

aortic stenosis because of the poor prognosis

SUMMARY OF
without surgery. Other causes include hypertrophic IMPORTANT POINTS
cardiomyopathy, primary pulmonary hypertension,
tetralogy of Fallot and left atrial myxoma.
In patients with a very recent onset of syncope, • Episodic loss of consciousness is usually due
to seizure or syncope.
additional causes to consider are:
• A detailed history, physical examination
• myocardial infarction including postural blood pressure, and 12
• pulmonary embolism lead ECG will establish the diagnosis in many
• aortic dissection, and cases of syncope and presyncope.
• pericardial tamponade. • Identifying cardiac disease is a priority
Mechanical causes are often suggested by history because the adverse prognosis can be
and examination findings and confirmed by stan- improved by appropriate treatment.
dard investigations such as chest X-ray, ECG,
ventilation perfusion scan (V/Q) and echocardiog-
raphy. All the cardiac causes of syncope are serious Conflict of interest: none declared.
and if a cardiac cause is suspected the patient
should be referred to a specialist. References
1. Sheldon R, Rose S, Ritchie D, et al. Historical criteria
Unknown cause that distinguish syncope from seizures. J Am Coll
Cardiol 2002; 40:142–148.
In the Framingham Study 37% of first episodes of 2. Soteriades E S, Evans J C, Carson M G, et al.
Incidence and prognosis of syncope. N Engl J Med
syncope were of an unknown cause.2 This group
2002; 347:878–885.
has a worse outcome compared to patients without 3. Brignole M, Alboni P, Benditt L, et al. Guidelines on
syncope, or with vasovagal syncope, with the management (diagnosis and treatment) of syncope.
adjusted hazard ratio for death 1.32 (95% CI: Euro Heart J 2001; 22:1256–1306.
4. Driving and heart disease. Task Force Report.
1.09–1.60).2 The adverse outcome may be due to Prepared on behalf of the Task Force by Petch M C.
unrecognised cardiac disease. Euro Heart J 1998; 19:1165–1177.
5. Austroads. Assessing fitness to drive. Victoria: ARRB,
Driving 2003; in press. AFP

Driver syncope is an uncommon cause of motor

vehicle accidents and specific guidelines have been
developed.4 New Australian guidelines, ‘Assessing
fitness to Drive’ are due to be released in 2003.5
For noncommercial drivers with neurally mediated
reflex syncope, ie. vasovagal episodes driving is
only restricted if symptoms are severe and uncon-
trolled. Specialist assessment is often required.

Conclusion
Dizziness and loss of consciousness are common
clinical problems. If the initial assessment suggests
REPRINT REQUESTS
presyncope or syncope as causing the symptoms, a
detailed history, physical examination including Dr Jeremy Wright
postural blood pressure and 12 lead ECG will Department of Cardiology
establish the diagnosis in many cases. Identifying Royal Perth Hospital
cardiac disease is a priority because of its adverse Box X 2213 GPO
prognosis. There are continuing advances in the Perth, WA 6847
diagnosis and treatment of syncope. Email: [email protected]

210 • Reprinted from Australian Family Physician Vol. 32, No. 4, April 2003