DIZZINESS, SYNCOPE, AND PRESYNCOPE
From the American Academy of Family Physicians’ Scientific Assembly, presented October 2007
Mary Elizabeth Roth, MD, Associate Chief, Academic Office, Department of Medical Affairs, Sacred Heart
Hospital, Allentown, PA
Educational Objectives
| The goal of this program is to improve the management of dizziness and syncope. After hearing and assimilating
this program, the clinician will be better able to:
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 | 1. Select medications for the vomiting patient with vertigo and tinnitus.
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| 2. List diagnostic components of Meniere’s disease.
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| 3. Describe the association of psychiatric disorders with syncope.
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| 4. Determine the need for echocardiography in patients with syncope, based on clinical findings.
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| 5. Evaluate patients with exertional syncope.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a
proprietary business or commercial interest. For this program, the following has been disclosed: Dr. Roth is a consultant and
serves on the advisory board for Eli Lilly and Company. The planning committee reported nothing to disclose.
Acknowledgments
Dr. Roth was recorded in Chicago, IL, at the 2007 Scientific Assembly, presented October 3-6, 2007, by the American
Academy of Family Physicians (AAFP). The Audio-Digest Foundation thanks Dr. Roth and the AAFP for their cooperation
in the production of this program.
| Definitions: vertigo—illusion or hallucination of motion; ≈50% of new complaints of dizziness associated with vertigo;
patient may fall or stagger; near syncope—feeling of impending faint; one-sixth of patients complain of dizziness; no
loss of consciousness or change in mental status; patient may fall or stagger; syncope—fainting or loss of consciousness
with loss of body tone; seizure—neurologic discharge; causes change in mental or physical status; patient may have dizziness
before, during, or after event; lightheadedness or dysequilibrium—gait disorder; involves feeling of falling or
staggering; causes include extrapyramidal disorder (eg, Parkinson’s disease, spondylosis, vitamin B12 deficiency); medications
and medication changes cause dizziness; inform patients that dizziness, numbness, tingling, gastrointestinal disturbances,
headache, sweating, anxiety, and sleep disturbances frequently associated with discontinuation of medication
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| Managing patient with vertigo at home: identify person to help patient; be concerned about hydration if vertigo
lasts >6 hr (find out when vertigo and vomiting started, and how long patient without fluids); consider padded mat to line
bathroom if episode prolonged; review patient’s medications list and determine what patient has available at home, or
contact pharmacy that delivers medications; if vertigo and vomiting lasts >6 hr, consider transferring patient to emergency
department (ED); relieve panic and improve function; negotiate care over telephone; tinnitus and diplopia—
advise patient to turn on music, lie with noisiest ear down on pillow, close eyes, and stay still; start with safe fast medications
(eg, 1 mg of diazepam [eg, Valium]; repeat in 30 min); proceed on to transdermal scopolamine patches if necessary;
consider later use of meclizine (eg, Antivert) as “bedtime sleeper”; some cases may be treated with anticholinergic drugs
(cause sleepiness and other side effects); in rare cases, patients may have perilymphatic fistula; management—patient
should rest for 48 to 72 hr until episode resolves; patient needs clear fluids immediately; use small doses of benzodiazepine
bid or tid; combination of agents can be used; patient should not drive when using acute doses; since agents can
mask refractory vertigo and rare diseases, they must be used short-term; place soft cervical collar or wrap Turkish towel
around patient’s neck to reduce neck movement; patient should return for follow-up ≤7 days later
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| Sudden unilateral hearing loss associated with acute vertigo: consider methylprednisolone; in patients with
unilateral acute vestibular neuronitis with acute loss of hearing and acute onset of vertigo with no central neurologic
symptoms, use of steroid in first 3 days associated with greater recovery (ie, normal hearing and no prolonged vertigo) at
1 yr
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| Office visit for dizziness: patient history—clarify sensation (eg, spinning, fainting, or falling) and positional effects
(eg, dizziness with standing or walking); ask about loss of consciousness, loss of hearing, ataxia, focal neurologic deficits,
and medications started at onset of symptoms; vestibular neuronitis associated with medications; physical
examination—check eardrum (usually normal); check orthostatic blood pressure (BP) and pulse; check gaze and head
shaking; perform Hallpike’s maneuver; rule out new murmurs and bruits; cerebellar and focal neurologic examination;
further work-up for true syncope or any cardiovascular (CV) abnormality (eg, arrhythmia); red flags—focal neurologic
deficit; new murmur (perform echocardiography); abnormal cardiac rhythm (perform immediate electrocardiography
[ECG]); if patient has vertical beating nystagmus or neurologic abnormality, consider neural imaging; some patients continue
to have vertigo or unexplained dizziness for 4 to 6 wk (consider, eg, depression, anxiety, and somatoform disorders);
refer for vestibular testing if patient continues to have nystagmus and true vertigo
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| Recurrent vertigo: causes—benign positional vertigo; Meniere’s disease; ruptured lymphatic vestibular bulb; tumor;
seizure; perform Hallpike’s maneuver; refer to audiologist for treatment using Epley maneuver; if symptoms last >2 wk,
worsen with time, or occur with greater frequency, refer to neurotologist; if central cause (ie, other neurologic symptoms)
suspected, look for metabolic causes and acoustic neuromas; laboratory work-up—erythrocyte sedimentation rate;
rheumatoid factor; antinuclear antibody (ANA) testing; lipid profile; rapid plasma reagin (RPR) testing (sudden hearing
loss associated with gumma); complete blood cell count (CBC); thyrotropin; audiometric evaluation to assess eighth
nerve and to differentiate between central and peripheral vertigo
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| Clinical pearls related to vertigo: review history of vertigo and tinnitus; examine patient; stop medications that aggravate
cochlea or acoustic nerve; remove cerumen; take history of industrial and military noise; review algorithm; consider
referral to otolaryngologist if no improvement; check nose and sinuses; assess cranial nerve and cervical spine;
neurologic testing; hyperventilation testing if psychiatric disorder suspected; examine eyes
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| Meniere’s disease: components include vertigo, diplopia, sense of ear blockage, and hearing loss; patients may have hyperacusis;
symptoms include fluctuating hearing loss (usually unilateral); hearing loss increases over time, especially
without intervention; tinnitus—fluctuates; sound usually starts in one ear without external cause; type and intensity of
sound varies; persistent tinnitus causes paranoia; pitch may be high or low; may exist in deaf patients (“it’s a sensation”);
sense of fullness or plugged ear; may be painful; fluctuating rotational vertigo—sense that world spinning around patient;
resolves when patient closes eyes; results in nausea and vomiting; atypical Meniere’s disease with no rotational vertigo
(cochlear hydrops); drop attack—sudden acute rotational vertigo causes patient to drop to ground as “world seems
to spin around them”; vomiting; can last minutes to hours (if >6 hr, patients require hydration in ED); after episode subsides,
patient may sleep for hours; may occur frequently or once per year; common precipitants of episodes—alcohol
use; high salt diet; sleep deprivation; stress; fatigue; overworking; high altitude; excess multidimensional motion; medications
(eg, nitrofurantoin); management—stabilize and educate patient while waiting for otolaryngology consultation
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| Syncope: dizziness, presyncope, and vertigo do not result in loss of consciousness or postural tone; patients who require
cardioversion to regain consciousness defined as having survived cardiac arrest (not syncope); ask about prodromal
symptoms, foods eaten, medications taken, and symptoms accompanying episode; determine whether patient lost consciousness
before falling; syncope causes temporary loss of consciousness due to sudden decline in blood flow to brain;
can occur in otherwise healthy people; patient feels faint, dizzy, or lightheaded (presyncope); accounts for 3% of ED visits
and 6% of hospital admissions in United States; warning signs—association with exercise; palpitation or irregularity
of heart; positive family history of syncope, recurrent syncope, or sudden death; can be associated with myoclonic jerks
(distinguish by tilt-table testing or electroencephalography [EEG]); high-risk patients—age >60 yr with positive history
of CV disease (CVD) who then have syncope; physical examination suggesting congestive heart failure (CHF); cardiac
outflow obstruction, aortic stenosis, murmur, or idiopathic hypertrophic subaortic stenosis (IHSS); low-risk patients—
age <45 yr with no CVD or other risk factors; patients with suspected reflex or vasovagal syncope; obtain 12-lead ECG
in patients with syncope when history and physical examination do not provide diagnosis; hospital admission for 24-hr
observation—syncope with documented loss of consciousness; positive history of CHF or any ventricular arrhythmia;
chest pain or symptoms compatible with acute coronary syndrome; evidence of CHF or valvular heart disease on physical
examination; new CHF; any ECG finding of ischemia, arrhythmia, prolonged QT interval, or bundle branch block; consider
in patients >60 yr of age with syncope, patients with history of coronary artery disease or congenital heart disease,
patients with history of myocardial infarction (MI) at, eg, age 46 yr, patients with positive family history of sudden death;
younger (<45 yr of age) patients with exertional syncope without obvious benign etiology; laboratory studies indicated if
syncope due to loss of circulating volume; if monitoring during 24-hr hold does not provide diagnosis and heart disease
suspected, consider electrophysiologic testing; in patients with palpitations, ECG and echocardiography recommended as
first step; in patients with chest pain, full work-up for CV risk recommended
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| American Heart Association recommendations: most children and young adults with syncope have no structural
heart disease or significant arrhythmia; extensive medical work-up rarely needed; careful physical examination (including
BP and heart rate [HR] measured lying and standing) generally only evaluation required
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| Recurrent syncope: patients require tilt-table testing and echocardiography; in older patients, consider trial of carotid
sinus massage; in patients with syncope occurring with neck turning, evaluate carotid sinuses early
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| Psychiatric disorders: potential causes of syncope; consider in young patients who faint frequently, patients in whom
syncope does not cause injury, and in patients who present with many symptoms (eg, nausea, fear, dread); patients often
have panic attacks; induce symptoms with hyperventilation testing; check postural BP; integrate evaluation of Diagnostic
and Statistical Manual of Mental Disorders IV (DSM-IV) axis I disorders (eg, anxiety, depression) with ability to
diagnose axis III medical disorders (eg, syncope, cardiac disease); 35% of patients with syncope have coexisting psychiatric
disorder, 9.2% have alcohol dependence; patients with psychiatric disorders and syncope tend to be younger, generally
do not have underlying heart disease, and have more frequent and dysfunctional syncope than cardiac patients;
evaluate risk for anxiety and depression in patients with recurrent syncope after 1 yr
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| Lung ventilation-perfusion (V/Q) scanning: reserved for patients in whom pulmonary embolism (PE) likely; syncope
and PE can result in loss of consciousness; perform on patient who recently underwent surgery or who is at risk for
PE; risk for syncope due to PE low unless patient has thrombophilia, on medication, recently underwent surgery, or has
postcancer syndrome; glucose tolerance testing rarely indicated because hypoglycemia uncommon cause of syncope
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| Neurally mediated syncope (NMS): when rhythmic movements seen (eg, clonic or myoclonic jerks), seizure frequently
diagnosed, but syncope can cause similar motions; distinguish via EEG (sleep and awake); consider neurocardiogenic
syncope (common in young people); NMS—appears similar to seizure and syncope; benign; common cause of
fainting; can mask life-threatening conditions; common in children and young adults but can occur at any age; work-up
required; results in loss of consciousness; occurs most often while standing; nausea; lightheadedness with visual grayout;
prolonged episodes can trigger seizure; place patient in reclining position to restore blood flow; if ECG and cardiac testing
normal, perform tilt-table testing (patients become symptomatic); monitor BP and HR; if ECG abnormal or positive
family history of sudden death syndrome, check QT interval for QT syndrome; exercise stress testing, Holter monitoring,
and echocardiography may be needed if patient has abnormalities or cause of NMS not identified; if tilt-table testing abnormal
in young patient with >1 episode of NMS and normal ECG, further work-up (eg, Holter monitoring) required; patients
must avoid dehydration and maintain blood volume; recommend frequent small meals with adequate salt intake;
watch for warning signs of fainting
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| Hospitalization: not required in many patients with syncope after careful history taken; patients need follow-up over
time; in patients with syncope of unknown origin, inpatient monitoring (with continuous ECG) for 24 hr warranted; if patient
has primary conduction disorder, nonsustained ventricular tachycardia, or possible pacemaker malfunction, inpatient
monitoring for 24 to 48 hr indicated; invasive electrophysiologic testing not necessarily warranted for all patients
until arrhythmic cause ruled out
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| Recommendations for echocardiography: class I evidence—highest level of evidence; perform echocardiography
in any patient with syncope and suspected heart disease or syncope with exertion; class IIa evidence—
echocardiography recommended for patients in high-risk occupations (eg, crane operators, pilots); class IIb evidence—
echocardiography reasonable in patients with syncope of occult etiology (ie, no findings of heart disease and on history
and physical examination); carotid massage—can be performed in absence of bruits, ventricular tachycardia, recent
stroke, or recent MI; diagnosis positive if patient asystolic for 3 sec; can be replaced by inpatient telemetry; perform
echocardiography in acute episode of syncope with suspicion of embolic disease, atrial fibrillation, or other risk (eg, transient
ischemic attack [TIA]); consider echocardiography with any neurologic findings; patient with neurologic event and
intrinsic cerebrovascular disease should undergo echocardiography; class III evidence—echocardiography not recommended
for patients in whom results of echocardiography would not alter approach to diagnosis or treatment, patients
with no clinical suspicion of heart disease, and patients with classic neurogenic syncope
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| Exertional syncope: echocardiography should be performed to rule out hypertrophic cardiomyopathy; exercise stress
testing may induce cardiac event; exercise stress testing should be done in patients who have syncope not while exercising,
and to evaluate ischemia or exercise-induced tachyarrhythmia; postexertional syncope—tilt-table testing most effective
for NMS associated with postexertion; tilt-table testing, echocardiography, and 24-hr hold for continuous ECG
monitoring “backbones” of syncope evaluation; perform exercise stress testing if no yield on tilt-table testing and
echocardiography if patient has exercise-associated syncope; look for exercise-induced ischemia, valvular heart disease,
PE, pulmonary hypertension, and neurologic signs and symptoms of syncope
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| Summary: start with history, physical examination, and ECG; if syncope exertional, perform echocardiography (if no
diagnosis reached, consider tilt-table testing and exercise stress testing); neurologic testing—if neurologic syncope
suspected, perform EEG; consider computed tomography (CT), magnetic resonance imaging (MRI), or carotid and transcranial
Doppler ultrasonography if patient has neurologic findings at time of syncope or postsyncope; small percentage
of patients identified for neurologic testing (patients must have history of seizure, prolonged loss of consciousness,
diplopia, headache, and postictal symptoms); if no abnormal reflexes seen on focal examination, brain imaging studies
not warranted; elderly patients with near syncope should be admitted for monitoring unless benign etiology clearly
identified (age associated with morbidity and mortality in near syncope); principles of syncope and near syncope—
evaluate dizzy patient; patients require thorough history and physical examination with focused laboratory and cardiac
testing; remove risk and panic and improve function; reassure patient’s family patient safe to be in home (may require
24-hr observation); help patient understand etiology of orthostatic hypertension, vertigo, syncope, and near syncope; review
history, medications, and new symptoms
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Suggested Reading
Brignole M et al: Task force on syncope, European Society of Cardiology. Part 2: Diagnostic tests and treatment
summary of recommendations. Europace 3:261, 2001; Colivicchi F et al: Exercise-related syncope in young competitive
athletes without evidence of structural heart disease. Clinical presentation and long-term outcome. Eur Heart J
23:1125, 2002; Freeman R: A treatment for neurally mediated syncope? (Don't) hold your breath. Ann Neurol
63:265, 2008; Giada F et al: Psychiatric profile, quality of life and risk of syncopal recurrence in patients with tilt-induced
vasovagal syncope. Europace 7:465, 2005; Gracie J et al: The role of psychological factors in response to
treatment in neurocardiogenic (vasovagal) syncope. Europace 8:636, 2006; Hilton M et al: The Epley (canalith repositioning)
manoeuvre for benign paroxysmal positional vertigo. Cochrane Database Syst Rev 1:CD003162, 2002;
Johnson EG: The dizziness dilemma. Addressing a problem that affects 40% of the population. Rehab Manag 20:25,
2007; Kouakam C et al: Prevalence and prognostic significance of psychiatric disorders in patients evaluated for recurrent
unexplained syncope. Am J Cardiol 89:530, 2002; Linzer M et al: Diagnosing syncope. Part 1: Value of history,
physical examination, and electrocardiography. Clinical Efficacy Assessment Project of the American College of
Physicians. Ann Intern Med 126:989, 1997; Macleod D et al: Vertigo: clinical assessment and diagnosis. Br J Hosp
Med (Lond) 69:330, 2008; Marques F et al: Recurrent syncope—a diagnostic challenge. Rev Port Cardiol 25:431,
2006; Radtke A et al: Screening for Menière's disease in the general population—the needle in the haystack. Acta
Otolaryngol 128:272, 2008; Recchia D et al: Echocardiography in the evaluation of patients with syncope. J Gen Intern
Med 10:649, 1995; Seemungal BM et al: A practical approach to acute vertigo. Pract Neurol 8:211, 2008;
Tonnessen GE et al: The value of tilt table testing with isoproterenol in determining therapy in adults with syncope
and presyncope of unexplained origin. Arch Intern Med 154:1613, 1994.
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