syncope evaluation and management jayne barr, md clinical assistant professor the ohio state...

SYNCOPEEVALUATION AND

MANAGEMENT

Jayne Barr, MD

Clinical Assistant Professor

The Ohio State University

Case #1

• 42 year old female

• Chief complaint: passing out at work

• Works in a pharmaceutical lab. Was sitting at her desk, felt nauseated and knew she was going to pass out.

• Per witnesses, was slump over chair and was unconscious for a few seconds.

Case continues

• No chest pain, palpitations, shortness of breath

• Similar episodes 10 years ago.

• No family history of sudden cardiac death

• No medications.

• No smoking. No alcohol. No drugs.

Case #2

• 82 year old male.• Found unresponsive by his son• Past medical history—HTN• Medications—HCTZ • Exam—BP 160/98. P 70. Now alert and

oriented. Facial contusions. Otherwise normal exam.

Q: How would you manage these 2 patients?

Syncope: Definition

• Abrupt and self-limited loss of consciousness associated with absence of postural tone

• Relatively rapid onset. Variable warning symptoms.

• Followed by rapid and complete recovery. Last only a few minutes.

• Absence of prolonged confusion• Presyncope---prodromal symptom of fainting

and typically has the same work up as syncope.

Significance of Syncope

• “The only difference between syncope and sudden death is that in one you wake up”. [1]

• --anonomymous

Syncope: Epidemiology

• 20-50% of adults experience at least one episode of syncope during their lifetime.

• Explained 53-62%• Infrequent, unexplained 38-47%

• 500,000 new syncope patients each year. • 3-5% of ER visits.• 6% of hospital visits.• More common in the elderly.

• Up to 23% in age >70 years.

Syncope: Economic Burden

• Per recent data, the overall cost per hospital admission was estimated to be about $10,600.

• One study found to be $17,000 of “unnecessary” testing to diagnosis vasovagal syncope

• Overall cost in US estimated to be in excess of $1 billion.

• Costs of Test• Troponin $78• EKG $221• Telemetry $255/d• Head CT $1545• MRI brain $2216• Carotid US $1294• EST $2492• Echocardiogram $809• EEG $1115

Causes of Syncope

Morbidity and Mortality

• Most cases benign.• Syncope of cardiac origin

has the highest morbidity and mortality.

• 1 year mortality of 18-33%

• Recurrence in the elderly population is 30%

• Syncope of unknown origin.

• 1 year mortality of 6-12%.

Syncope in Children

• Generally a benign event.

• Most common causes– Vasovagal (40%)– Simple faint (29%)– Breathholding (4%)– Unknown (15%)

• Rare but serious causes of syncope in children – Hypertrophic

cardiomyopathy– Anomalous origin of left

coronary artery– Myocarditis– Long QT syndrome– Cystic medial necrosis– WPW

Syncope: Pathophysiology• Decreased cerebral

perfusion is common to all causes of syncope

• Cessation of cerebral perfusion for as little as 3-5 seconds can result in syncope

• Decreased cerebral perfusion may occur as a result of decreased cardiac output or decreased systemic vascular resistance.

More Pathophysiology

• Bilateral hemisphere dysfunction or reticular activating system (RAS) midbrain knockout.

• Generally acute hypoperfusion is responsible.– Regional

(vasoconstriction)– Systemic (global

hypotension)

• Loss of consciousness causes loss of postural tone leading to collapse

• 35% reduction in cerebral blood flow will cause syncope.

• Modifying factors– Cardiac output– Systemic and local vascular

resistance/occlusion– Blood volume– Ability to compensate

Syncope: Etiology

• Mnemonic: PASSOUT• P-ressue (hypotensive causes)• A-rrthymias• S-eizures• S-ugar (hypo/hyper glycemia)• O-utput (cardiac)/ O2 (hypoxia)• U-nusual causes• T-ransient (TIAs, strokes, CNS diseases)

More specifics

• OUTPUT– Cardiac

• AS, PA, MS,IHSS• Cardiomyopathies• Atrial myoxomas• Cardiac tamponade• Aortic dissection• MI, CHF

– Pulmonary• PE, acute hypoxemia• Pulmonary HTN• COPD exacerbation• CO poisoning

• UNUSUAL CAUSES• Anxiety, Panic disorder• Major depressive disorder• Somatization disorder

(psychogenic syncope)• Hyperventilation syndrome• Migraine, sleep disorder

• TRANSIENT• TIA (vertebrobasilar), CVA,

subdural hematoma• Subarachnoid hemorrhage• CNS mass effect (tumor)• Basilar artery migraine.

Syncope

• CAUSES (Head---Heart---Vessels)– Reflex mediated

• Vasovagal, carotid sinus, situational

– Cardiac • Mechanical , arrhythmias

– Orthostatic • Drugs, autonomic failure

– Cerebrovascular – Unknown– Nonsyncopal causes

Neurally mediated reflex syncope (36-62%); average (24%)

• Vasovagal, carotid sinus, situational

• No increased risk for cardiovascular morbidity or mortality associated with reflex mediated syncope.

Neurally Mediated Reflex Syncope--what happens?

• Stress causes an abnormal autonomic reflex

• Normal increased sympathetic tone replaced by increased vagal tone

• Variable contribution of vasodilation and bradycardia.

• Examples include syncope from:– Pain and/or fear– Carotid sinus hypersensitivity– “situational” (cough,

micturition, defecation syncope)

Vasovagal syncope

• Most common cause of syncope in young adults

• Precipitating event is often identifiable– Stress, trauma, pain,

sight of blood, prolonged standing, heat exposure

Vasovagal Syncope

• 3 PHASES• --Prodrome

• Diaphoresis, epigastric discomfort, weakness, nausea, dizziness

• Lasts about 2 minutes

• --Loss of consciousness• Usually lasts 5-20 seconds

• --Postsyncopal phase• Nausea, dizziness, general sense of poor health• If present, confusion which lasts no more than 30 seconds

Prevalence of VasoVagal Syncope

• Prevalence poorly known (8-37% with mean of 18%)

• Important points– Patients with VVS younger than Carotid sinus

syndrome patients– Age range teens to elderly with mean 43 years– Pallor, nausea, sweating, palpitations are common– Amnesia for warning symptoms in older patients

Vasovagal Syncope Management

Management for Vasovagal syncope

• Optimal management is source of debate– Patient education, reassurance, instruction– Fluids (sports drinks), salt, diet– Tilt training– Support hose (waist high)

• Drug therapies

• Pacing (DDD pacing)– Class II indication if positive tilt test and

cardioinhibitory or mixed reflex

Drug therapies for Vasovagal syncope

• Salt/volume– Salt, sports drinks,

fludrocortisone• Beta-adrenergic blockers

– 1 positive control study using atenolol

– Use if hx of htn

• Disopyramide• SSRIs

– 1 controlled study– Use if hx of depression

• Vasoconstrictors (eg, midodrine)– 1 negative controlled study

(etilephrine)– ? Efficacy of

neosynephrine– Use midodrine if

significant hypotension

Postural Orthostatic Tachycardia Syndrome

• Upright symptoms without hypotension.• Upright tachycardia—excessive HR response

to maintain a low normal BP. • 500,000 Americans, usually young women• Partial dysautonomia• Antecedent infection, surgery, pregnancy• Treatment—low dose propanolol 10mg tid

Carotid Sinus Syncope

• Syncope related to head turning, shaving, wearing a tight collar

• Pathophysiology– Carotid sinus

pressure causes a reflex decrease in heart rate and blood pressure

Carotid sinus massage

• Site– Carotid arterial pulse just

below thyroid cartilage

• Method– Massage, not occlusion.– Right followed by left,

pause between– Duration:5-10 seconds– Posture: supine and erect

• Risks– 1/5000 massages

complicated by TIA

• Outcome– 3 sec asystole and/or

50mmHg fall in systolic blood pressure with reproduction of symptoms ==CAROTID SINUS SYNDROME

• Contraindications– Carotid bruit, known but

significant carotid arterial disease, previous CVA, MI last 3 months.

Situational Syncope

• Related to micturition, defecation, swallowing or coughing

• Induced by baroreceptor and mechanoreceptors causing vagal stimulation

• Circumstances of the event are typically diagnostic

Orthostatic syncope

• When vertical, blood follows gravity and pools.• Increased sympathetic tone counteracts this.• If the response is inadequate, syncope occurs.• Drop in BP: 20 systolic or 10 diastolic within 3

minutes of standing• Present in 40% of patients over 70 years old• May be due to

– Drugs– Volume loss– Neurologic damage

More on Orthostatic Hypotension

• Volume loss– Assoc. with tachycardia

• Medications– Seen in elderly 45% of

time

• Situational– Micturition, cough,

postprandial, carotid sinus sensitivity, defecation, laughing

• Adrenal insufficiency

• Primary autonomic disease– Idiopathic, parkinsons

disease, multisystem atrophy (Shy-Dragger)

• Secondary autonomic disease– Neuropathic (dm, amyloid,

alcoholism, autoimmune, vitamin deficiency, etc)

– CNS (cva, MS, tumors, spinal cord)

Cardiac Syncope

• Two basic types– Dysrhythmia mediated– Structural

cardiopulmonary lesions

• Both cause the heart to be unable to sufficiently increase cardiac output to meet demand

• Double the risk of mortality compared with other syncopal patients. Up to 50% mortality.

• Patients with underlying cardiac disease are at greatest risk for cardiac syncope. Only 3% have no previous heart disease.

• Cardiac arrythymias especially in the elderly have high mortality.

Neurologic Syncope

• Rarely the primary cause of syncope• Ischemia to the RAS in the brainstem may cause

“drop attacks”• Results from Vertebrobasilar insufficiency due to TIA

(sometimes basilar migraine)• Usually accompanied by vertigo, ataxia, dysarthia,

diplopia

• Other examples• Subclavian steal—occurs with arm activity. Systolic BP in arms

(difference of 10mmHg)• Subarachnoid hemorrhage

Psychiatric causes

• Most commonly associated with• Anxiety• Panic• Major depressive disorders

• Variety of mechanisms may be involved• Hyperventilation• Increased vagal tone

Syncope-like States

• Migraine• Acute hypoxia• Hyperventilation• Somatization disorder (psychogenic syncope)• Acute intoxication (ie alcohol)• Seizures• Hypoglycemia• Sleep disorders

An Approach to Syncope

P sych o lo g ica lE va lu a tion

H e a d C T sca n / S ku ll f ilm sC a ro tid D o p p le r

M R I b ra inE E G

N e u ro lo g ica lE va lu a tion

E N TE va lu a tion

H o lte r/E L R /ILRT ilt T a b le

E ch oca rd io g ramE P S

C a rd io va scu la rE va lu a tion

A n g io g ramE xe rc ise te st

O th erC a rd io va scu la r

te sting

E n d oc rineE va lu a tion

H is to ryP h ys ica l E xam

E K G

HISTORY

• RAPID ASSESSMENT– Identify Life-Threatening causes

– Dysrhythmias– cardiac ischemia– Critical aortic stenosis– Aortic dissection– Pulmonary embolus– CVA– SAH– Toxic-metabolic derangement

HISTORY

• HISTORY alone identifies the cause up to 85% of the time

• POINTS– Previous episodes– Character of the events, witnesses– Events preceding the syncope– Events during and after the episode

HISTORY

• Events preceding the syncope– Prolonged standing

(vasovagal)– Immediately upon

standing (orthostatic)– With exertion (cardiac)– Sudden without warning or

palpitations (cardiac)– Aggressive dieting– Heat exposure– Emotional stress

• Events during and after the episode– Trauma (implication

important)– Chest pain (CAD, PE)– Seizure (incontinence,

confusion, tongue laceration, postictal behavior)

– Cerebrovascular syndrome (diplopia, dysarthia, hemiparesis)

– Associated with n/v/sweating (vasovagal)

HISTORY• Associated symptoms

– Chest pain, SOB, lightheadedness, incontinence

• Past medical history– Identifying risk factors– Morbidity and mortality

increases with organic causes

• Parkinsons (orthostatic)• Epilepsy (seizure)• DM (cardiac, autonomic

dysfunction, glucose)• Cardiac disease

• Medications– Antihypertensives,

diuretics (orthostatic)– Antiarrthymics (cardiac

syncope)– TCA, Amiodarone

(cardiac/prolonged QT)

• Family history– Sudden death (cardiac

syncope/prolonged QT or Brugada)

PHYSICAL EXAM

• Vital signs– Orthostatics—most

important• Drop in BP and fixed HR -

>dysautonomia• Drop in BP and increase

HR -> volume depletion/ vasodilatation

• Insignificant drop in BP and marked increase in HR -> POTS

– Temperature• Hypo/hyperthermia (sepsis,

toxic-metabolic, exposure)

– Heart rate• Tachy/brady, dysrhythmia

– Respiratory rate• Tachypnea (pe, hypoxia,

anxiety)• Bradypnea (cns,

toxicmetabolic)

– Blood pressure• High (cns, toxic/metabolic)• Low (hypovolemia,

cardiogenic shock, sepsis)

PHYSICAL EXAM

• HEENT– Tenderness/deformity

(trauma)– Papilledema (increased

icp, head injury)– Breath (alcohol, dka)

• NECK– Bruits– JVD (chf, mi, pe,

tampnade)

• HEART– Murmur (valves,

dissection)– Rub (pericarditis,

tamponade)

• LUNGS– Sounds may help

distinguish chf, infection, pneumothorax

PHYSICAL EXAM

• ABDOMEN– Pulsatile mass; AAA– Tenderness– Occult blood loss

• PELVIS– Bleeding, hypovolemia– Tenderness (PID, ectopic,

torsion, sepsis)

• SKIN– Signs of trauma,

hypoperfusion

• EXTREMITES– Paralysis (CNS)– Pulses unequal

(dissection, embolus, steal)

PHYSICAL EXAM

• NEUROLOGIC– Mental status; toxic

metabolic; organic disease; seizure; hypoxia.

– Focal findings (hemorrhagic/ischemic stroke, trauma, tumor, or other primary neurologic disease

– Cranial nerves– Cerebellar testing

Seizure or Not?

• SEIZURE– Frothing at mouth– Tongue biting– Disorientation/ postictal– Age < 45 year– LOC over 5 minutes

*tongue biting found only in seizure (99% specificity); absence did not exclude the possibility of a seizure (24% sensitivity)

• NOT A SEIZURE– Sweating prior to

episode– Nausea prior to

episode– Oriented after event– Age > 45 years

Ancillary Studies

• EKG---Cornerstone of workup– Arrhythmia, long qt, WPW, conduction abn.

• Routine Blood work—limited value• Radiology---limited value except if abnormal

exam• Other tests—depending of history and exam

– Glucose --hemoglobin --troponin– Ua/culture --CK (syncope vs seizure)

Starting the “Workup”

• If young adult and No comorbid conditions or symptoms

Most likely VASOMOTOR or ORTHOSTATIC .

*Clinicians may forego the EKG in young, healthy patients with an obvious cause of syncope.

Normal EKG

• If Normal EKG:– Check orthostatics– Check hemoglobin

• If low---Anemia• If normal or high--Volume loss, dehydration, drug

induced

Young adult, no comorbidity, normal EKG, absent orthostatics

• Vasomotor– Try carotid massage

• (+) carotid sinus sensitivity

• (-) reflex or neurocardiogenic

• Metabolic– Check chemistry.

R/O hypoglycemia, adrenal insufficiency

• Neurologic– CT head (tia, cva, sah)– EEG (if suspect Sz)

• Cardiovascular– If Outflow obstruction,

check CT chest, Echo (PE, valvular, HOCM)

– If venous return, check HCG, Echo (pregnancy, tamponade)

The EKGKey Points

• Guidelines recommend EKG in the evaluation of all patients with syncope.

• Exception: young healthy patients with an obvious cause of syncope

• Abnormal EKG in 90% of patient with cardiac syncope

• Only 6% of patients with reflex mediated syncope have abnormal EKG.

• Syncopal patient with negative cardiac history and normal EKG—unlikely to have a cardiac cause

The EKG patient older, +comorbid signs/symptoms

• If Abnormal EKG– Ischemia/injury– Dysrhythmia

• Sinus brady, BBB, AV block, prolonged QT, WPW, HOCM, Brugada

• If Normal EKG– Consider holter or event recorder if

dysrhythmia suspected

WPW

sinus bradycardia ventricular tachycardia 3 or more beats

Prolonged QT interval

Other: sinus pause> 2 sec, SVT, afib, 2nd or 3rd AV block, PM malfunction

Summary of the CardiovascularDiagnostic Pathway

T re a t

P o s it ive

T ilt ta b leE L R /ILR

N e ga tive

E ch oca rd io g ramE P S

K n o w n S truc tu ra lH e a rt D ise a se

T ilt ta b leIL R

> 3 0 d a ys> 2 e ven ts

tilt ta b leH o lte r/E LR

IL R

< 3 0 d a ys

N o S tru c tu ra lH e a rt D ise a se

H is to ryP h ys ica l E xam

E K G

S Y N C O P E

Holter Monitoring

• 24-48 hour monitor—limited value because of intermittent nature of arrhythmias

• Event recorder—more helpful. Patient must be conscious in order to activate unit.

• Establishes diagnosis in only 2-3% of patients with syncope if EKG is normal.

• Indicated in patients at highest risk for arrhythmia ie, abnormal ekg, palpitations, cad history, syncope when supine or with exertion, +FH

Holter results--summary

• PACs and PVCs– Usually not significant– Exception: ie 3 consecutive 3 PVCs at 100 bpm

• Bigeminy—may be significant• AV block---is important• Bradycardia---if signs and symptoms correlate

Loop Event Recorders

• Provides longer monitoring—weeks to months• Can activate the monitor after symptoms occur,

thereby freezing in its memory the readings from the previous 2-5 minutes and the subsequent 1 minute

• In patients with recurrent syncope, arrhythmias were found during symptoms in 8-20%.

• Limitations: compliance, use of device, transmission

ECHOCARDIOGRAM

• Access structural causes of cardiac syncope– AS, MS, HOCM, atrial myoxoma

• Unlikely to be helpful in the absence of known cardiac disease or an abnormal ekg.

• INDICATIONS– Abnormal EKG ---history of heart disease– Murmur ---exercise assoc.

syncope

Structural Heart Disease

• Aortic Stenosis– Most common structural lesion associated

with syncope in the elderly

• Hypertrophic Obstructive Cardiomyopathy– Vasodilatation (drugs/hot bath) can induce

syncope

• Obstruction to Right Ventricular Outflow– PE, pulmonary stenosis, pulmonary htn

EXERCISE STRESS TEST

• Syncope during exercise is more likely to be related to an arrhythmia

• Post-exertional syncope is usually neurally mediated.

• Echocardiogram should be done prior to EST to r/o structural abnormality.

• INDICATION– Syncope during or shortly after exercise

(exertional syncope)

EPS—Intracardiac EPS

• Rarely indicated in patients with structurally normal hearts and normal ekg.

• Diagnostic yield greatest in patients with known heart disease but non-diagnostic ekg monitoring.

• Heart disease-------50-80%• No heart disease---18-50%

• Difficult to correlate spontaneous events and laboratory findings

• Ineffective for assessing bradyarrhythmias

• Often must settle for an attributable cause

• Abnormal finding on EPS does not guarantee that this was what caused the patient’s syncope.

• EPS is abnormal in 18-68% of patients with syncope of unknown cause.

EP testing—Useful Diagnostic findings

• Inducible monomorphic VT• Sinus node response time > 3000 ms or

carotid sinus response time >600 ms• Inducible SVT with hypotension• HV interval > 100ms (especially in

absence of inducible VT)• Pacing induced infra-nodal block

TILT TABLE TEST

• Changes in position to reproduce symptoms of the syncopal event.

• Positive tilt table test– Induction of bradycardia

and hypotension– Considered diagnostic for

vasovagal syncope

Indications for Tilt table test

• Unexplained recurrent syncope or syncope associated with injury in absence of structural heart ds.

• Unexplained recurrent syncope or syncope associated with injury in setting of organic heart disease after exclusion of potential cardiac cause of syncope

• Identification of neurally mediated syncope could alter treatment

• Evaluation of recurrent unexplained falls.

• Evaluation of near syncope or dizziness

Tilt Table Test

• Unmasks Vasovagal syncope susceptibility

• Reproduces symptoms• Positive Tilt Test

*Prophylaxis treatment—beta blockers or disopyramide as well as SSRIs

*Recurrent symptoms and bradycardia may require pacemaker

NEUROLOGIC TESTING

• Tend to be overused• Includes EEG, CT head, MRI head, Carotid

dopplers• In contrast, Cardiovascular tests are

underused.• INDICATION

– Only if history and physical exam suggests a neurologic cause or testing for other causes is complete.

EEG

• Not a first line of testing

• To differentiate syncope from seizure

• Abnormal EEG in the interval between two attacks -> Epilepsy

• Normal EEG -> does not tell us anything

Tests and Diagnostic Yield Test/procedure yield (%)

history and physical 49-85

EKG 2-11

EPS without SHD 11

EPS with SHD 49

Tilt table test without SHD 11-87 (syncope pt +TTT 24-75%)

Ambulatory EKG

holter 2

loop recorder 2-3wks 20

implantable LR upto 14mo 65-88

Neurological (ct, carotid) 0-4

Syncope Evaluation Flow Chart

Syncope Evaluation Flow Chart

When to Admit

• Consider admitting if age greater than 40 years• Discharge if benign etiology

– Vasovagal, micturition, psychogenic syncope

• Admit if – Suspected or known significant heart disease ie cardiac

ischemia, CHF, structural heart ds or +family hx of SCD– EKG suggestive of arrhythmia or syncope during exercise– Stroke– Syncope causing severe injury– Severe orthostatic hypotension

ACEP guidelines

Clinical Risk Score for Predicting 1 year Mortality in Patients with Syncope

• Risk Factors– Abnormal ekg– Age >45 years– History of CHF– History of ventricular

arrhythmia

Number of risk factors

1 year mortality (%)

0 1

1 9

2 16

3/4 27/80

Congestive Heart Failure

• CHF = poor outcome– N=491; 12% with syncope– Cardiac syncope; 49% dead 1 year– Noncardiac syncope; 39% dead 1 year– No syncope; 12% dead 1 year

*CHF is a risk factor for poor outcome in multiple studies

San Francisco Syncope Rule

• Risk Factors– C History of CHF– H Hematocrit less than 30– E Non-sinus rhythm or new changes in EKG– S Systolic BP less than 90– S Shortness of breath

• Predicting Serious Outcome (at 7 days)– Low risk (no risk factor)---0.3% serious outcome– High risk (1+risk factor)---15.2% serious outcome

Predictor of 30 day serious events in older patients with syncope

• Predictors of increased risk– Age >90y, male gender, arrhythmias, SBP> 160,

abnormal EKG, Abnormal troponins

• Predictor of decreased risk– Near syncope

• Stratified in low (0), intermediate (1-2) and High (>2) risk groups.

• CHF was not associated with increased risk• Even low risk group—2.5% risk • Needs validation Annals Emerg Med 2009.

Driving and Return to Work

• Vasovagal syncope---can return to work

• VT---no driving for 3-6 months

• In Ohio, can not be a Commercial Driver if diagnosed with syncope

Case #1 Continues

• Physical exam: Normal• Orthostatics: Normal• EKG: Normal• Labs: no anemia. Glucose normal.• ECHO: Normal• Tilt Table Test: after 7 minutes of 70 degrees

upright, HR 36, BP 51/41, LOC. Regained consciousness with supine position.

Case #1 Conclusion

• DIAGNOSIS----Vasovagal Syncope

• TREATMENT---Florinef, Ted hose, Fluids

• OUTCOME---No reoccurence of symptoms when followed up at 3 months, 6 months, and 1 year later.

Case #2 Continues

• Emergency Room workup—negative. Electrolytes, CBC normal. EKG showed NSR with occasional PVCs.

• Decision made to ADMIT.• 2 hours later---Nonsustained Vtach.• EP study—Inducible Vtach. Automated internal

defibrillator placed.• Cardiac cath---diffuse coronary artery disease.

SUMMARY

• Syncope is a transient loss of consciousness due to decreased cerebral blood flow.

• Most common causes: vasovagal, cardiac (cardiac arrhythmia), and orthostatic hypotension. Seizures are rare.

• Patients with cardiac syncope are at increased risk of death.

• History and Physical exam are the MOST important to identify the cause

• Orthostatic BPs should be done on all pts.

SUMMARY

• Shotgun approach is Not helpful.• EKG should be considered in all patients.• Tilt table test can diagnosis vasovagal syncope.• Neurologic testing is low yield and often

overused.• Holter monitoring, Echo, EST, EP considered in

patients at high risk for cardiac syncope.• Patients remain undiagnosed in 34% of cases.

Clues to the Etiology of Syncope

• Cough, micturition, defecation, swallowing---situational syncope

• Syncope with arm exercise---subclavian steal• Syncope with shaving---carotid sinus syncope• Syncope with change of position---orthostatic• Prodromal symptoms (nausea, diaphoresis)---

neurally mediated reflex (vasovagal)

Clues to the Etiology of Syncope

• Syncope with exertion---AS, IHSS, arrhythmias• Abrupt onset---cardiac syncope• Blood pressure/pulse differential---Aortic

dissection, subclavian steal syndrome• Post-syncopal disorientation; incontinence---

seizure

REFERENCES

• Engel. Ann Internal Med. 1978. 89; 403-412

• Kapor, W. Medicine. 1990. 69; 160-175.• Krahn. Cardiology Clinic. 1997• ACEP Clinical Policy on Syncope.• Ann Emerg Med. 2009.• Mayo Clinic Proceedings. Nov 2008.