syncope work-up in primary care - peacehealth ohvi... · syncope work-up in primary care ramakota...
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Syncope Work-up in Primary Care
Ramakota K. ReddyCardiac Electrophysiology.
Sept 24, 2011
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2
Disclosures• Paid Consultant: St. Jude, Medtronic• Speaker: Sanofi-Aventis, Boeringher-Ingleheim• Research Support: Medtronic, St. Jude
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Objectives• Review the differential diagnosis of syncope• Review the diagnostic value of various tests
used in syncope• To be able to initiate a thoughtful and directed
workup for the patient with syncope• To gain an understanding of neurally mediated
syncope
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What is Syncope?
• A syndrome consisting of a relatively short period of temporary and self limited loss of consciousness.
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The Significance of Syncope
1 National Disease and Therapeutic Index on Syncope and Collapse, ICD-9-CM 780.2, IMS America, 19972 Blanc J-J, L’her C, Touiza A, et al. Eur Heart J, 2002; 23: 815-820.3 Day SC, et al, AM J of Med 19824 Kapoor W. Evaluation and outcome of patients with syncope. Medicine 1990;69:160-175
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Frequency of Syncope
• Spans all age groups– < 18 y/o 15%– 17-26 y/o 25% (military)– 40-59 y/o 16% (male), 19% (female)– Nursing home 23%
Lipsitz LA. Queensland J Med. 1985;55(216):45-54.Savage DD. Stroke. 1985;16(4):626-629.Campbell et al: Age and Aging 1981;10:264-270
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Anxiety/depression 73%1
Daily life activities 71%2
Driving 60%2
Physical activities 56%2
Employment 37%2
Sexual function 30%2
Relationships with family, spouse, friends 28-30%2
1 Linzer M. J Clinical Epidemiol. 1991;44:1037-1043.2 Linzer M, et al. J Gen Intern Med. 1994;9:181-186.
Recurrent, Unexplained Syncope: Quality Of Life Impact
Area of Impairment
Proportion Impaired
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Why do we all Hate Syncope?
• An occasional patient will have something bad• Diagnostic workup is hard
– History is the key diagnostic tool but no one trusts it – “Objective” tests are often non-diagnostic or worse
• The most common form of syncope occurs in healthy people and is often dramatic
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Classification of Syncope
• Neurally mediated• Orthostatic• Cardiac arrhythmia• Structural / Obstructive• Cerebrovascular• (Psychiatric)• (Not Syncope)
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Neurally Mediated Syncope
• This is an active reflex• Vasovagal Syncope (trigger = postural stress)• Situational Faint
– Cough, Sneeze, Micturition, Defecation, Swallowing, Post prandial, Emotional, Post-exercise, Pain, Post-operative
• Carotid Sinus Hypersensitivity
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Examples of “Vagal” Syncope
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Orthostatic Syncope
• This is a passive process• Primary Autonomic Failure Syndromes
– Pure Autonomic Failure– Mulitsystem Atrophy (Shy-Drager)– Parkinson’s Disease– ? POTS
• Secondary Autonomic Failure– DM, drugs, Alcohol, Amyloid, MS, GBS
• Volume Depletion
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Cardiac Arrhythmias
• Bradycardia– Sinus Node dysfunction– AV block
• Tachycardia– Structurally abnormal heart (CHF, etc)– Electrically abnormal heart (LQT, Brugada, etc)
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Structural / Obstructive
• Valvular disease• HOCM• Aortic dissection• Atrial Myxoma• Pulmonary embolism• Pulmonary hypertension
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Cerebrovascular
• Vascular Steal Syndrome• Vertebro-basilar insufficiency• Basilar artery migrane
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Psychiatric Diagnosis• May account for up to 35% in referral population• Diagnosis
– Generalized Anxiety
– Panic
– Major Depression
– EtOH
– Conversion
• Usually with high rate of recurrence• 60% of pts with hyperventilation syncope have an
underlying psychiatric diagnosis.
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Syncope vs Epilepsy
• Lampert study in 59 German med students• 12% had tonic-clonic type movements, 80%
myoclonic– Brief– After LOC– Not really tonic-clonic (gross flailing, random,
contraction of axial muscles, non-rhythmic)
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Syncope vs TIA
• Syncope: Transient loss of consciousness without neurological deficit
• TIA: Transient neurological deficit without loss of consciousness
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Syncope-like States
• Migrane*• Acute Hypoxemia*• Hyperventilation*• Somatization disorder (psychogenic syncope)• Acute Intoxication (e.g., EtOH, drugs)• Seizures• Hypoglycemia• Sleep disorders* May cause ‘true’ syncope
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Relative Incidence of Causes:Unselected patients presenting to the ER
Neurally Mediated
Arrhythmia
Obstructive
Orthostatic
Hysteria
Unknown Other
Neurologic
1 Grubb, Olshansky (eds). Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co., Inc., 1998, p.1
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Workup of Syncope
“Medicine is an art of certainty and a science of probability.”
- Sir William Osler
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Diagnostic Testing in Syncope• History & Physical Examination
– Most valuable test– Diagnostic Yield: 35-40%
• Other generally useful tests– Echocardiogram– Resting ECG– Ambulatory ECG (Loop recorder)
• Rarely useful– MRI, CT, Dopplers, EEG, EP study, Treadmill
• Controversial: Tilt table test
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History & Physical
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
Is This Syncope?
• Is there loss of consciousness?• Is it transient & self-limited?• Was it Intoxication, Drugs,
Hypoxia or Falling asleep?• Was there continued
confusion/disorientation for >5 minutes after regaining consciousness?
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History & Physical
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
Neurological Findings?
• Are there focal neurological deficits on exam?
• Was there a migrane type headache?
• If no findings, you do not need MRI, CT, dopplers, EEG, etc.
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History & Physical
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
Orthostatic Hypotension?
Is the patient Orthostatic?– Not all patients will show orthostatic
tachycardia
• Does the patient have any of the medical conditions predisposing to Orthostatic Hypotension?
• Are there predisposing drugs?• Is there is suggestion of
dehydration?
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Orthostatic Hypotension Characteristics
• Syncope after arising rapidly• May be sudden in elderly• Recurrent episodes or persistent pre-
syncope• May occur in elderly after large meals• Other Manifestations of autonomic
dysfunction
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History & Physical
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
Is it Obviously Vagal?
• If typical vagal episode, diagnosis can be purely clinical
• Carotid Sinus Massage in elderly can be diagnostic
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History Pearls: Vagal• Pre-event
– Stereotypical Trigger (Postural, cough, micturition, etc)
– Nausea, diaphoresis, feeling warm, pale
• Recovery– Simultaneous recovery of consciousness and orientation
– Persistent nausea, urge to defacate, weak/lightheadedness
– Post recovery can feel lousy for hours and faint again
– Pallor
• Post-LOC “seizure” = NON-neurological event– Usually vagal. Sometimes hysterical.
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Residual Differential
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
Assess Prognosis
• Is it high risk?• If NOT:
– Syncope will likely still recur, but sudden death is unlikely
– Reassure patient– Make diagnosis clinically or by
recording an ambulatory event– Outpatient workup
• Echocardiogram
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Assessing prognosis: Worrisome Findings
• Resting ECG– Long QT interval
– Heart block
– Prior infarction
– Bundle Branch Block
• History– During exercise (NOT after)
– Severe ambient chest pain
– Unheralded, Complete recovery
– Patient looks/feels fine afterwards
– Family Hx of premature SCD
• Echocardiogram– LV dysfunction
– RV dysplasia
– Aortic stenosis
– Pulmonary hypertension
– Myxomas, other weird stuff
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Unexplained Syncope
Neurally MediatedOrthostaticArrhythmicObstructiveCerebrovascularPsychiatricNot Syncope
About 40% of cases
• Good prognosis• Would like an ECG with event
– 1st episode: Wait for more or loop monitor
– Frequent episodes: Loop recorder (Holter only if daily episodes)
– Infrequent episodes: Consider implantable event monitor
– Consider: Tilt, Psych eval
• May remain undiagnosed…
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History Pearls: Unexplained syncope
• Family history– Consider LQT syndromes, HCM
• Palpitations suggest:– Sinus tachycardia from volume depletion,
hypoglycemia or vasodilation– Hyperventilation, psychiatric, vagal– PSVT (rare to occur without palpitations)– Sick Sinus Syndrome (A-fib then pause)– VT (Often occurs without palpitations)
• Psychiatric history
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Diagnostic Yield (%) of Individual Testsin Work-up of Syncope, pre-Tilt Table Testing
% WithClinical Recurrent Neuro-
Author (N) Setting Syncope H&P ECG Holter CSM EPS logic Other Total
Eagle (100) Inpatient 33 52 — 3 — 0 2 4 61
Day (198) ER 37 73 2 2 — — 9 — 87
Silverstein (108) MICU — 39 — 7.5 — — — 6.5 53
Kapoor (204) In- and 68 25 6 14 — 1.5 0.5 5 52(1983) outpatient
Martin (170)* ER — 53 1 3 — — 5 — 62
Kapoor (433) All 49 32 7 13 1 2 1 3 41(1990)*
*Prospective study
Chang-Sing P. Cardiol Clinics. 1991;9(4):641-651.
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Diagnostic Tests: Provocative• Tilt Table Test
– False positive rate 10-25%
– Should only be considered positive if clinical symptoms are reproduced
– Tests for “empty heart” vagal episodes, not other neurally mediated syncopies. False negative rate can be high.
• Electrophysiology Testing– Yield for Bradycardia: <50%
– Tachycardia: Unknown yield, but negative test gives a prognosis equal to patients who have similar heart disease but did not have syncope.
– Rarely helpful in patients with normal LV, ECG
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Diagnostic Tests: True Clinical• Holter Monitor• Ambulatory Event Recording (surface or implanted)• Implantable Loop Recorder
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Diagnostic Tests: Ambulatory ECG recording
• Holter Monitor– 4% Symptoms with arrhythmia True Positive– 15% Symptoms and no arrhythmia True Negative– 14% Arrhythmia but no symptoms Confusing– 65% No arrhythmia, no symptoms Non-diagnostic
• Loop Monitor (ambulatory event monitor) x 1 month– 20% Symptoms and arrhythmia True Positive– 27% Symptoms and no arrhythmia True Negative– 53% No symptoms Non-diagnostic
• Implanted loop monitor now available
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Holter placed when patient had a clinical episode of atrial fibrillation
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Value of Event Recorder in Syncope
Linzer M. Am J Cardiol. 1990;66:214-219.
*Asterisk denotes event marker
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Implantable loop recorder
• Allows prolonged (14 month) recordings with long pre-event looping memory.
• Patient activated and automatic triggers• Implantation procedure <20 minutes
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ILR Recordings*56 yo woman with syncope accompanied
with seizures.Infra-Hisian AV Block: Dual chamber
pacemaker
65 yo man with syncope accompanied with brief retrograde amnesia.
VT and VF: ICD and meds
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Summary: Syncope
• Frequent symptom often resulting in expensive, extensive workup and much patient and physician angst.
• History is critical.• Prognosis depends on existence of cardiac
disease, regardless of actual diagnosis.• Shotgun diagnostic approach is unrewarding• Therapy is diagnosis dependent
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Neurally Mediated SyncopeA detailed look
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Word Jumble• Common Faint• Vagal syncope• Vasovagal syncope• Neurocardiogenic sycope• Vasodepressor syncope• Neurodepressor syncope• Cardiodepressor syncope
• Situational syncope• Micturation Syncope• Cough Syncope• Defecation Syncope• Swallow Syncope• Carotid Sinus
Hypersensitivity (?)
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Neurally Mediated Syncope:Common Misconceptions
• It is a fancy name for orthostatic syncope• It is a diagnosis of exclusion• If syncope is bad enough, it can’t be just vagal• It only affects the young• It’s not a “real” diagnosis
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Characteristics of Neurally Mediated Sycnope
• Very symptomatic, alarming, events– Pale, sweaty, chest pain– Feels like a heart attack to the patient– Sometimes associated with “seizure” activity– Patients do not believe it is benign
• Recurrent• Young healthy patient thinks you are ignoring a
very serious life-threatening problem• Almost all tests will be negative
– Reinforces patient’s perception that it is serious
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Neurally Mediated Syncope• Clinical sequence of events:
– Trigger of some sort: Postural, Situational, PVC, Vasodilator
– Variable period of nausea, epigastric discomfort, weakness, pallor, diaphoresis, lightheadedness
– Loss of consciousness often with tonic or tonic-clonic seizure like movements (convulsive syncope)
– Recovery of consciousness when supine
– Persistent nausea, weakness for several minutes. Often urge to have a BM
• May recur quickly if patient tries to stand up too soon
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Neurally Mediated Syncope
• Pathophysiology– Active reflex– Afferent limb can be variable
• Endocardial stretch receptors, GI stretch receptors, dorsal motor nucleus of vagal nerve, pulmonary irritation, pain receptors, central, smooth muscle receptors
– Efferent limb• Removal of all sympathetic tone• Profound vagal input to heart leads to asystole
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Neurally Mediated Syncope: Triggers
• “Empty Heart” (endocardial stretch receptors)– Hypovolemia, hyperdynamic (post-PVC)– Emotional, sight of blood, pain
• Glossopharyngeal (dorsal motor nucleus)• Micturation or defecation syncope (smooth
muscle stretch receptors)• Swallow Syncope (stretch receptors in esoph)
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Pathopysiology of Posturally TriggeredNeurally Mediated (Vagal) Syncope
Mosqueda-Garcia, et al. Circulation 2000; 102:2898-2906.
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Tilt Table Test for Syncope• Used to unmask postural neurally-
mediated syncope
• Measure heart rate and blood pressure in supine & 70° head-up tilt positions for 30-60 mins
• Isoproterenol infusion or Nitroglycerine pharmacological stress sometimes
• Patient often learns warning symptoms (“tilt training”)
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Classification of Abnormal Responses to Tilt Table Testing
• Cardio-inhibitory (mainly bradycardia)
• Vasodepressor (marked hypotension without marked bradycardia)
• Mixed (hypotension with bradycardia)
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Head-Up Tilt Test (HUT)
DG Benditt, UM Cardiac Arrhythmia Center
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Implantable Loop Recording: Vagal Syncope
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Use of the Tilt Table Test
• NOT all patients with neurally mediated syncope
• When patient doesn’t believe your clinical diagnosis and demands a test
• Recurrent syncope (especially with injuries)• Failure of initial therapy
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Vagal Syncope: Treatment• Reassure• Eliminate “Empty Heart” Trigger
– Volume/Salt loading– Beta Blockers– Disopyramide– Florinef
• Blunt Efferent limb of reflex– Midodrine– Pacing
• ? Mechanism– Paxil
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Pacing helps in unblinded trials
• Vasovagal Pacemaker Study (VPS-1)• VASIS
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VPS- I
Connolly S, et al. J Am Coll Cardiol 1999; 33: 16-20.
CumulativeRisk(%)
100
90
80
70
60
50
40
30
20
10
015129630
Control (No Pacemaker)
2P=0.000022
Pacemaker
Time in Months
NumberAt Risk
C 27 9 4 2 1 0P 27 21 17 12 11 8
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Blinded Trials: Minimal Benefit
• SYNPACE• VPS-2
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0.4
0.3
0.2
ODODDD
P = 0.153 (one-sided)
Number at Risk ODO 40 37 35 32 31 21DDD 39 36 34 33 33 17
0 1 2 3 4 5 6
0.1
0.0
Cum
ulat
ive
Ris
k of
Sy
ncop
e
Presented at the 23rd Annual Scientific Sessions of the North American Society of Pacing and Electrophysiology. Late Breaking Clinical Trials, May 11, 2002.
VPS-II: Phase I
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Pacing conclusions
• Pacemaker implantation can help somepatients with NMS
• Pacer therapy guided by results of Tilt table testing fails to show benefit in blinded randomized trials
• Even patients who don’t have syncope after pacing will (>90%) have pre-syncope symptoms.