SYNCOPE EVALUATION 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 historyHTN MedicationsHCTZ ExamBP 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 EKG Telemetry Head CT MRI brain Carotid US EST Echocardiogram EEG

$78 $221 $255/d $1545 $2216 $1294 $2492 $809 $1115

Causes of Syncope

Morbidity and Mortality

Most cases benign. Syncope of cardiac origin has the highest morbidity and mortality.
1 year mortality of 1833%

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 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

Pulmonary

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

Disopyramide SSRIs
1 controlled study Use if hx of depression

Beta-adrenergic blockers
1 positive control study using atenolol Use if hx of htn

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 tachycardiaexcessive HR response to maintain a low normal BP. 500,000 Americans, usually young women Partial dysautonomia Antecedent infection, surgery, pregnancy Treatmentlow 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

Outcome
3 sec asystole and/or 50mmHg fall in systolic blood pressure with reproduction of symptoms ==CAROTID SINUS SYNDROME

Method
Massage, not occlusion. Right followed by left, pause between Duration:5-10 seconds Posture: supine and erect

Contraindications
Carotid bruit, known but significant carotid arterial disease, previous CVA, MI last 3 months.

Risks
1/5000 massages complicated by TIA

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

Primary autonomic disease

Idiopathic, parkinsons disease, multisystem atrophy (Shy-Dragger)

Medications
Seen in elderly 45% of time

Situational
Micturition, cough, postprandial, carotid sinus sensitivity, defecation, laughing

Secondary autonomic disease

Neuropathic (dm, amyloid, alcoholism, autoimmune, vitamin deficiency, etc) CNS (cva, MS, tumors, spinal cord)

Adrenal insufficiency

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 stealoccurs 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
History Physical Exam EKG

Neurological Evaluation

ENT Evaluation

Cardiovascular Evaluation

Other Cardiovascular testing

Endocrine Evaluation

Head CT scan/ Skull films Carotid Doppler MRI brain EEG

Holter/ELR/ILR Tilt Table Echocardiogram EPS

Angiogram Exercise test

Psychological Evaluation

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

Medications
Antihypertensives, diuretics (orthostatic) Antiarrthymics (cardiac syncope) TCA, Amiodarone (cardiac/prolonged QT)

Past medical history

Identifying risk factors Morbidity and mortality increases with organic causes
Parkinsons (orthostatic) Epilepsy (seizure) DM (cardiac, autonomic dysfunction, glucose) Cardiac disease

Family history
Sudden death (cardiac syncope/prolonged QT or Brugada)

PHYSICAL EXAM
Vital signs
Orthostaticsmost 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

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)

Temperature
Hypo/hyperthermia (sepsis, toxic-metabolic, exposure)

PHYSICAL EXAM
HEENT
Tenderness/deformity (trauma) Papilledema (increased icp, head injury) Breath (alcohol, dka)

HEART
Murmur (valves, dissection) Rub (pericarditis, tamponade)

NECK
Bruits JVD (chf, mi, pe, tampnade)

LUNGS
Sounds may help distinguish chf, infection, pneumothorax

PHYSICAL EXAM
ABDOMEN
Pulsatile mass; AAA Tenderness Occult blood loss

SKIN
Signs of trauma, hypoperfusion

PELVIS
Bleeding, hypovolemia Tenderness (PID, ectopic, torsion, sepsis)

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 worklimited value Radiology---limited value except if abnormal exam Other testsdepending of history and exam
Glucose Ua/culture --hemoglobin --troponin --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

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)

Metabolic
Check chemistry. R/O hypoglycemia, adrenal insufficiency

The EKG Key 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 EKGunlikely 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

sinus bradycardia

ventricular tachycardia
3 or more beats

WPW

Prolonged QT interval

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

Summary of the Cardiovascular Diagnostic Pathway

SYNCOPE History Physical Exam EKG

Known Structural Heart Disease

No Structural Heart Disease

Echocardiogram EPS

>30 days > 2 events

< 30 days

Positive

Negative

Tilt table ILR

tilt table Holter/ELR ILR

Treat

Tilt table ELR/ILR

Holter Monitoring
24-48 hour monitorlimited value because of intermittent nature of arrhythmias Event recordermore 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

Bigeminymay be significant AV block---is important Bradycardia---if signs and symptoms correlate

Loop Event Recorders

Provides longer monitoringweeks 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 Murmur ---history of heart disease ---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)

EPSIntracardiac EPS
Rarely indicated in patients with structurally normal hearts and normal ekg. Diagnostic yield greatest in patients with known heart disease but nondiagnostic ekg monitoring.
Heart disease-------5080% No heart disease---1850%

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 patients syncope. EPS is abnormal in 1868% of patients with syncope of unknown cause.

EP testingUseful 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 history and physical EKG yield (%) 49-85 2-11

EPS without SHD

EPS with SHD Tilt table test without SHD

11
49 11-87 (syncope pt +TTT 24-75%) 2 20 65-88 0-4

Ambulatory EKG
holter loop recorder 2-3wks implantable LR upto 14mo Neurological (ct, carotid)

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 0

1

1 year mortality (%) 1

9

2
3/4

16
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 H E S S History of CHF Hematocrit less than 30 Non-sinus rhythm or new changes in EKG Systolic BP less than 90 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 group2.5% 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 workupnegative. Electrolytes, CBC normal. EKG showed NSR with occasional PVCs. Decision made to ADMIT. 2 hours later---Nonsustained Vtach. EP studyInducible 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; 403412 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.