Management of Syncope in the Emergency Department
Jonathon M. Sullivan MD, PhD
Honorary Professor Syncopatus Emeritus Bullshitticus Maximus Duplicitus
Department of Emergency Medicine
Wayne State University
DFO’S FOR DUMMIES
LIMITS AND BOUNDARIES
 Won’t talk about pediatric syncope
 What are these “children” things I keep hearing
about?
 Won’t parade a bunch of papers
 You’re welcome
 This isn’t an EKG conference
 Leave it to the Berkserker
 Outpatient workup of syncope
 About 50% Voodoo anyway
CASE STUDY:
 48 yo maladjusted WM EP w. no PMH has witnessed
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LOC while standing at pt bedside (work hour 13),
sustaining head injury.
Brief prodrome of fatigue, stress, dizziness,
sandwich-related thoughts.
Overcaffeinated, up for 16.5 hours, minimal food or
H2O due to workload.
No pulse palpated for about 5s, CPR briefly initiated.
Return of consciousness at 10-20 secs:
Slightly confused but appropriate:
 “Get the f**k up off me.”
 Exam shows a poorly-groomed middle-aged hump
with normal VS, congenital anisocoria (no burr holes,
please), small occipital scalp lac, CTA, RRR, normal
neuro, pulse ox 99%.
QUESTIONS:
 What are the immediate treatment/stabilization
priorities?
 Is this syncope or something else?
 Is the differential for syncope
 Quite Extensive,
 Humongoid, or
 Galactically colossal?
 What are the relevant historical and physical exam
findings?
 What tests, if any, would you order on this doofus?
 What is the best way to make this guy somebody
else’s problem?
IMMEDIATE PRIORITIES:
 This is 2009:
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Check insurance status
Register patient
Print stickers
Click 29-minute box
Use foam on entering module
 Handwashing Gestapo are everywhere
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Approach the customer with a bright DMC smile.
ABCs, monitor, O2, IV
C-spine precautions
Check glucose?
WAS THIS SYNCOPE?
 If so, why? If not, why not?
WHAT IS SYNCOPE?
 συγκοπή – “syncopa” to cut off.
 Cut off what?
 Greek guys didn’t say.
 Syncope = transient loss of consciousness and
postural tone with rapid onset and
spontaneous, prompt and complete recovery
without intervention.
 So: Did our patient have syncope?
WHAT COULD CAUSE SYNCOPE?
 Anything that causes a sudden, transient loss of
consciousness can cause syncope.
 Assumes that we know what consciousness is.
 Consciousness can report only its presence, not its absence.
 But that’s another lecture.
 In most people, the organ of consciousness is the
brain.
 Therefore, syncope is a manifestation of brain (endorgan) dysfunction.
 At the neurological level, only two things can cause
syncope:
 Transient brainstem dysfunction at the level of the RAS; or
 Transient bilateral cerebral dysfunction.
 This is a tall order! What could do this?
WHAT COULD CAUSE SYNCOPE?
 NEUROGENIC:
WHAT COULD CAUSE SYNCOPE?
 TOXIC-METABOLIC
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ALCOHOL
SEDATIVE-HYPNOTICS (HERON, ETC)
SYMPATHOMIMETICS (CAINE, CRANK, ETC)
AXE BODY SPRAY AND OTHER WHIFFERS
GLUCOSE
SODIUM
CALCIUM
POTASSIUM
HISTAMINE, ALLERGIC REACTIONS
HYPOXIA
WHAT COULD CAUSE SYNCOPE?
 CARDIOVASCULAR
 The critical organ system…
 …that constantly pumps…
 …the essential good stuff…
 …that makes the brains go.
 SUTTON’S LAW:
 “That’s where the money is.”
WHAT COULD CAUSE SYNCOPE?

CARDIOVASCULAR:

Arrhythmias
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Bradycardias
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
Tachycardias

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Left-sided: Hypertrophic cardiomyopathy, left atrial myxoma, aortic stenosis, mitrial stenosis
Right-sided: PE, pulm htn, pulmonic stenosis, right atrial myxoma
Valvulopathy
PE
Vascular Catastrophes

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
Malignant
“stable”
Think long QT, Torsades, SVT, VTach
Obstruction to flow

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Carotic sinus sensitivity
Sick sinus syndrome
Heart blocks
Pacemaker malfunction
Dissection
Ruptured AAA
Vasomotor
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Orthostasis and hypovolemia
Autonomic dysfunction
Situational syncope
Anaphylaxis—bee stings, scromboid, drug rxs, etc.
“Vasovagal syncope”
WHAT COULD CAUSE SYNCOPE?
 VASOVAGAL
 One of the most notorious wastebasket diagnoses
in clinical medicine.
 Derives from ignoramus
 An ancient Greek work meaning “doctor has no
f**k’n clue why you dfo’d.”
 More general (and therefore, usually, more
correct) term is neurocardiogenic syncope.
 Proximate cause is actually increased vasomotor
tone and cardiac contractility
WHAT COULD CAUSE SYNCOPE?
 VASOVAGAL
 Can occur in any susceptible patient when
precipitated by any event which causes:
 Venous pooling
 Increased sympathetic tone
 May be both caused (pooling) or exacerbated
(enhances reflex) by alcohol.
 Patients are fine immediately after precipitant (such
as standing), then dfo as reflex kicks in.
WHAT COULD CAUSE SYNCOPE?
 VASOVAGAL
VENOUS
POOLING
INC
SYMP’TIC
TONE
ALL KINDSA STUFF!
BETZOLDJARISH
REFLEX
BRADYCARDIA,
VENODILATION,
DFO
WHAT COULD CAUSE SYNCOPE?
 VASOVAGAL
WHAT COULD CAUSE SYNCOPE?
 VASOVAGAL
 High-Risk Diagnosis. Why?
 Because this is what you’ll put on the chart when you
send that guy home with the ruptured AAA.
 Don’t make the diagnosis of “vasovagal” unless you
have clear historical and exam findings to support it.
 In fact, try not to make this diagnosis at all. There’s
nothing wrong with a final impression of “syncope.”
 “You don’t have to make the right diagnosis. You just
have to make the right decision.”
 El-Rod
WHAT COULD CAUSE SYNCOPE?
 SITUATIONAL SYNCOPE
WHAT COULD CAUSE SYNCOPE?
 SITUATIONAL SYNCOPE
 Fear, pain, stress
 Hunger
 Unbearable sights
 Blood, vomit, filth
 Violence, death
 Fat people in spandex
 Elvis, Hitler, Brad Pitt
 Urination, defecation, sneezing, coughing, swallowing
 Decreased venous return/Valsava
 BJ reflex?
WHAT COULD CAUSE SYNCOPE?
 BY FREQUENCY (fr Henry et al):
 COMMON:
 VT, SVT
 Hypovolemia: bleed-ING from AAA, ectopic, GIB,
etc
 Vasovagal
 Situational: cough, micturition, defecation
 Drug-induced – usually cardioactive agents
WHAT COULD CAUSE SYNCOPE?
 BY FREQUENCY (fr Henry et al):
 LESS COMMON:
 PE
 Heart block
 Valvulopathy (stenosis)
 MI
 Pacemaker malfunction
 SAH
 Psychogenic
 Bradycardias
 Psychogenic
WHAT COULD CAUSE SYNCOPE?
 BY FREQUENCY (fr Henry et al):
 RARE (BUT IMPORTANT):
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Aortic dissection
Basilar migraine/TIA
Trigeminal or glossopharyngeal neuralgia
Sublcavian steal
Pulmonary hypertension
Atrial myxoma
WHAT COULD CAUSE SYNCOPE?
 SULLYDOG’S BOTTOM LINE:
 Toxic-metabolic – not unheard-of, especially with
cardio/vasoactive agents, but relatively
uncommon
 Neurogenic – extremely uncommon, especially in
the absence of persistent neurologic symptoms or
neuro findings
 Cardiovascular – Sutton’s law applies.
WHAT HISTORICAL AND EXAM
FEATURES ARE IMPORTANT?
 ALL OF THEM. SERIOUSLY.
 H&P is the key to risk stratification in syncope.
 HISTORY-Use eyewitnesses if available
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Duration of LOC
Possible precipitants, prodrome
Convulsions – not all that convulses is seizure
Trauma
Seated vs. standing
Disorientation after ROC
PMH, Medications, All, SHx, FHx
 Focus on hx of cardiovasc disease (esp CHF), vasoactive meds,
cns agents, diuretics, meds for ED, FHx of sudden death.
WHAT HISTORICAL AND EXAM
FEATURES ARE IMPORTANT?
 EXAM:
 They don’t call ‘em “vital signs” for nuttin’.
 Orthostatics—fuggedaboudit.
 No agreement on numbers; nobody does them right, especially in ED.
 Sens/Spec totally suck ass.
 Just think about it:
 Syncope is usually cardiovascular/vasomotor
 Orthostasics, if properly done and if positive, suggest either hypovolemia
(easily detected with history or other exam findings) or a
cardiovascular/vasomotor cause.
 So orthostatics help us make better decisions…how?
 Thanks for playing.
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Trauma-CHI, tongue biting, C-spine
Signs of CHF—big mortality correlation
Abdominal/rectal: Tenderness, occult blood, Big Red.
Neuro: absence of findings strongly argues against neurogenic
syncope.
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 Accu-check?
 Lytes, BUN, Cr/gluc, Ca, Mag, Phos, AST, ALT,
Amylase, Lipase, TFTs, PT/PTT, UA, UDS,
SDS, Lactate, Osms? Right?
 CT of the Brains?
 EKG?
 Chest x-ray?
 Orthostatics?
 Other?
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 Number One Rule:
Use your history and physical to guide testing.
What a concept, huh?
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 EKG
 Low yield, but
 Highly specific when positive
 Cheap, noninvasive, makes you look very doctor-y.
 Arrhythmias, blocks, pre-excitation syndromes, long QT,
Brugada, MI, LVH, etc.
 Monitor
 Oh, for crying out loud. Why wouldn’t you?
 May detect badness not seen on 12-lead snapshot
 4 factors suggest benefit of extended monitoring
 Old dudes, heart disease, nonsinus rhythm on EKG.
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 THE OBLIGATORY EKG SECTION
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 THE OBLIGATORY EKG SECTION
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 THE OBLIGATORY EKG SECTION
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 THE OBLIGATORY EKG SECTION
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 THE OBLIGATORY EKG SECTION
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 Rapid Glucose
 Who gets syncope from hypoglycemia?
 Nobody, that’s who.
 Remember the definition of syncope:
 Syncope = transient loss of consciousness and postural
tone with rapid onset and spontaneous, prompt and
complete recovery without intervention.
 How many hypoglycemics present like this?
 Test is cheap and safe, but diagnostic yield approaches
zero.
 Absolute indication:
 Attending tells you to get it.
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 OTHER LABS
 Yield is extremely low, unless used to confirm
specific suspicions raised by exam. Routine use is
not recommended anywhere in the current
literature. Caveats:
 All women are pregnant.
 All pregnant women have ectopics.
 Hct < 30% predicts adverse events.
 Of course, so does syncope.
 d-dimer in suspected PE w. syncope is loser-ness.
If you suspect PE + syncope, image.
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 IMAGING
WHAT TESTS WOULD YOU ORDER
ON THIS DOOFUS?
 IMAGING
 ACEP: “There is no evidence to suggest that
routine screening of syncope patients with
advanced imaging (such as CT), functional echo,
or EP testing is indicated.”
 No neuro findings on H&P + no CHI = no CT.
 Echo indicated only in patients with cardiac
disease, abnormal EKG, suspected aortic stenosis.
 Consider rapid US to screen for AAA in selected
patients.
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 SEVERAL QUESTIONS OBTAIN:
 Which patients with syncope will croak soon?
 REALLY soon: admit
 KINDA soon: close followup.
 Or admit. Whatever keeps your undies dry.
 Which patients with syncope need an outpatient
workup, and what kind of workup is that?
 Which patients with syncope, if any, need to just
get on with their lives?
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 THE NACHRUL HYSTERY OF SYNCOPE
PROGNOSIS EXCELLENT
NOT SO MUCH
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 THE NACHRUL HYSTERY OF SYNCOPE
 Actual data:
 Pts with cardiovascular cause have “strikingly
higher” incidence of sudden death
 Pts with CHF have high mortality whether or not the
CHF “caused” the syncope
 Translation: CHF is bad.
 Age > 65 = high mortality. (Ya think?)
 Abnormal EKG is NFG.
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 ACEP HIGH-RISK / ADMISSION FACTORS:
 “Older age” and associated comorbidities
 Hct < 30
 History or presence of CHF, CAD, or structural
heart disease
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 THE CHESS RULE (San Francisco Rule)
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CHF – pre-existing or new finding
Hematocrit < 30%
ECG Abnormality
Shortness of breath
SBP < 90 mmHg on arrivall
 Initial Validation Set promising
 Followup studies: not so much
 CHESS seems to be better at telling you who to
bring in than who to send home
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 OTHER “DECISION RULES”
 Boston Syncope Rules
 Remains to be validated
 25 frippin’ criteria!
 Mnemonic:
HOW CAN WE MAKE THIS GUY
SOMEBODY ELSE’S PROBLEM?
 WHO CAN GO HOME?
 Patients who don’t need to be admitted.
 Young and otherwise healthy, no major comorbidities
 No neuro findings
 No cardiovascular history or findings, normal EKG
 No evidence of bleedING, guaiac neg, Hct>30 (if checked)
 Targeted studies (eg, CTPA, US for ectopic, LP for SAH)
negative
 Good followup
 Sullydog
WHAT HAPPENED TO SYNCOPE
GUY?
WHAT HAPPENED TO SYNCOPE
GUY?
 EKG negative
 Head CT negative
 Labs negative
 Serial trops negative
 Perfusion stress negative
 Attitude negative
 No additional episodes
 1-year outcome pending
IS OUR DOCTORS LEARNING?
 LET’S REVIEW, SHALL WE?
 Syncope is a sudden, transient, self-limited loss of
awareness and postural tone caused by global (not
focal) dysfunction of the consciousness organ.
 In most of us, that’s the brain.
 Neurogenic and metabolic causes are very rare.
 Cardiovascular and vasomotor causes are very
common.
 Risk stratification and indications for admission and
testing come almost exclusively from H&P.
 Aside from Hct, routine lab tests are just about
worthless.
IS OUR DOCTORS LEARNING?
 LET’S REVIEW, SHALL WE?
 Routine imaging is very low yield. Targeted
imaging is useful.
 Admission criteria:
 Any Sick Old Geez with:

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Heart Dis-eeZ
Goofy EKG-eeZ
Low BP-eeZ
Suckin’ Wind/Wh-eeZE, or
Low CBC-eeZ.
 Now THAT’s a mnemonic.
IS OUR DOCTORS LEARNING?
 LET’S REVIEW, SHALL WE?
 The Sullydog Admission Rule:
 Old + Syncope = Admit.
 May not meet interqual admission criteria.
 Ask me later what I think about interqual admission
criteria.
 Lie to get them admitted if you have to.
 (Sullydog is a moral relativist.)
 Insert Heated Argument Here.
IS OUR DOCTORS LEARNING?
 LET’S REVIEW, SHALL WE?
 Discharge Criteria:
 Patient does not require admission.
VERY FUNNY