Formulation and Implementation Donald E. Katz, C.O., L.O. Kevin Felton, C.O., L.O.
Syncope - 2008 - Joe Marshall · Syncope: Pathophysiology •Transient (10 sec) cessation of blood...
Transcript of Syncope - 2008 - Joe Marshall · Syncope: Pathophysiology •Transient (10 sec) cessation of blood...
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December 17, 2008
Joe M. Moody, Jr, MD
UTHSCSA and STVHCS
I have no conflicts of interest related to this presentation.
Syncope - 2008
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Outline
• Epidemiology
• Etiology
• Assessment
• Management
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Role of Provider in Management
of the Patient with Syncope
• Provide answers to the patient
– Diagnosis – identification of cause
– Prognosis – risk of death
• Prevent death or disability
• Provide relief of symptoms –
improve patient’s quality of life
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Syncope is a Frequent Complaint
• Definition: Sudden loss of consciousness and
inability to maintain postural tone followed by
spontaneous recovery
• Syncope accounts for
– 1-3% of ER visits
– about 1% of hospital admissions
• Incidence of first episode of syncope is 6 per
1000 person/years (Framingham)
• Prevalence of syncope in persons >45 y.o. is
about 15-20% (closer to 20% in women and
15% in men; Mayo Clinic)
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Syncope Incidence, Framingham
Soteriades ES et al. N Engl J Med. 2002;347:878.
Overall 6% risk in 10 years
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Syncope: Etiology
• Vascular: orthostatic hypotension or
reflex-mediated syncope
• Cardiac: arrhythmia, obstructive disease
(valve, HCM, PE)
• Apparent syncope: neurologic causes
(seizure, cerebrovascular insufficiency)
• Apparent syncope: metabolic causes
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Syncope: Pathophysiology
• Transient (10 sec) cessation of blood flow to reticular activating system of medulla, with spontaneous return
BP = C.O. * SVR
BP = (HR *S.V.) * SVR
Bradycardja
(sinus or AV
block)
Diastolic volume
Diastolic filling (pulm embolus)
Diastolic filling time (tachycardia)
Systolic function (aortic stenosis, etc.)
Reflex mediated
Orthostasis
Autonomic insufficiency
Medication, alcohol
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Neurocardiogenic Syncope
Chen-Scarabelli C et al. BMJ 2004;329:336.
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Syncope Incidence, Framingham
Soteriades ES et al. N Engl J Med. 2002;347:878.
Overall 6% risk in 10 years
Neuro-
cardiogenic,
Psychiatric,
Arrhythmia
(WPW, LQT)
Neuro-
cardiogenic,
Reflex,
Panic,
Orthostatic
Neuro-
cardiogenic,
Obstruction,
Heart
Disease
Circulation 2006:113:316.
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Framingham
Soteriades ES et al. N Engl J Med. 2002;347:878
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Syncope Prognosis,
Framingham
Soteriades ES et al. N Engl J Med. 2002;347:878
6.5 8.7 16.2
Cardiac Neurol
50%
Normal and Vasovagal
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Evaluation of the Patient:
The “Five-finger” Approach
of Dr. W. Proctor Harvey
History
Physical Signs
ECG
X-Ray
Diagnostic Laboratory
W. Proctor Harvey, April 19, 1918 to September 26, 2007
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AHA/ACC Scientific Statement - Evaluation of
Syncope. Circulation 2006:113:316.
Syncope
Workup
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Aspects of the History in the
Patient Presenting with Syncope
• Note: The history is the most important
contributor to a correct diagnosis
• The history
– The days and hours before the event
– The prodrome and precipitants
– The episode and consequences (injury)
and the recovery
AHA/ACC Scientific Statement - Evaluation of
Syncope. Circulation 2006:113:316.
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Days and Hours Before the Event
• Recent immobilization or injury
(pulmonary embolism)
• Change in medication (orthostatic
hypotension, proarrhythmia)
• Recent illness or decreased fluid intake
• Heat exposure, dehydration
AHA/ACC Scientific Statement - Evaluation of
Syncope. Circulation 2006:113:316.
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Prodrome in Syncope
• Feeling of heat, lightheadedness,
sweating, pallor, or nausea or vomiting
– neurocardiogenic
• No prodrome (or <5 sec) – arrhythmia,
autonomic dysfunction with hypotension
• Aura or premonition – seizure
• Palpitations – arrhythmia,
neurocardiogenic
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Precipitants in Syncope
• Standing or after exercise – neurocardiogenic or
postural hypotension
• During exercise – cardiac, neurocardiogenic
• Seated or reclining – cardiac
• Loud noise or extreme stress in young - cardiac
• Noxious stimulus, pain or fear – neurocardiogenic
• Turning of head, shaving or tight collars – carotid
sinus hypersensitivity
• Deglutition, micturition, defecation, cough, laugh –
reflex syncope
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The Clinical Setting in Syncope
• Age forms an important context
• Prior head trauma might indicate neurologic cause (seizure)
• Prior cardiac history or current cardiac symptoms (coronary, valvular, myocardial, or congenital disease)
• Family history of syncope or sudden death (in family member <30 yo), especially in young patients
AHA/ACC Scientific Statement - Evaluation of
Syncope. Circulation 2006:113:316.
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The Event and Sequelae
• Observations by onlookers often provide critically important information – tonic-clonic seizure activity can occur both with true seizure and with cardiac and neurocardiogenic causes of syncope
• No sequelae – arrhythmia, orthostatic hypotension
• Fatigue, nausea, weakness – neurocardiogenic
• Postictal confusion or focal neurologic symptoms – neurologic
• Injury is present in about 1/3, no diagnostic significance
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History to Distinguish Syncope
from LOC due to Seizure• Waking with cut tongue after spell +2
• Prodrome of déjà vu or jamais vu +1
• LOC with emotional stress +1
• Head turn to one side during LOC +1
• Unresponsive, posturing, jerking limbs, no recollection during LOC +1
• Confusion after LOC +1
• Lightheaded spells -2
• Diaphoresis before LOC -2
• LOC with prolonged stand or sit -2
• Score ≥1 is Seizure with accuracy 85%
• Score <1 is Syncope
Sheldon, R et al. J Am Coll Cardiol. 2002;40:142.
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Evaluation of the Patient:
The “Five-finger” Approach
History
Physical Exam
ECG
Chest X-Ray
Other Tests
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Physical Examination in the
Patient with Syncope• Vital signs – orthostatic BP at 3 minutes, check
femoral pulses, heart rate, regularity of rhythm
• Head trauma – tongue biting, esp. unilateral
• Cardiovascular – jvp, bruits, LV heave, RV lift, heart sounds (loud P2), gallops, murmurs (AS, MS, tumor plop)
• Abdominal pain or tenderness
• Neurologic – cognition, speech, visual fields, motor strength, tremor, gait
• Bedside maneuvers – carotid sinus massage, Valsalva maneuver (autonomic function)
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Evaluation of the Patient:
The “Five-finger” Approach
History
Physical Exam
ECG
Chest X-Ray
Other Tests
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ECG Abnormalities in Syncope(helpful in about 5%)
• Bifascicular block or IVCD (QRS >0.12 sec)
• Mobitz I (Wenckebach) AV block (?1st AVB)
• Asymptomatic sinus bradycardia (<50) or SA
exit block or pause (>3 s) in absence of
negative chronotropic medications
• Delta wave – WPW and tachyarrhythmia
• Long QT interval, Brugada syndrome
• Arrhythmogenic RV cardiomyopathy
• Signs of heart disease – MI, (hypertrophy)
Brignole M. et al. Eur Heart J. 2004;25:2054-72.
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Arrhythmic Causes of
Syncope
Bradyarrhythmia
Tachyarrhythmia
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Syncope and Bradyarrhythmias
• About 2/3 of patients with syncope due to arrhythmia are due to bradyarrhythmia (AV block more than sinus node dysfunction)
Sinus pause
Junctional escape
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Second Degree AV Block,
Wenckebach (Mobitz I)
0.32 0.38 block 0.32 0.400.32 0.40 0.45 block
2:1 2:1
V1
II
3:2
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easy
Second Degree AV block, 2:1
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• Not so easy… could misdiagnose as NSR rate 64.
• But actually is sinus tachycardia at rate of 128 (patient is
likely sick) with 2:1 block.
• The extra P waves are best seen at the 3 red arrows, and
are same shape and axis as the sinus P waves.
• Wide QRS indicates disease below the bundle of His.
Second Degree AV block, 2:1
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Second-Degree AV Block, Mobitz II• Intermittent blocked P waves
• PR interval constant for conducted beats
• Most are associated with BBB
• About 1/3 of patients with Mobitz II have block located in the His
bundle, so QRS is narrow
• Rarely Mobitz II is due to block in the AV node
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Third Degree AV block
(Complete Heart Block)
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The Three Authors
Wolff-Parkinson-White
Louis Wolff
Sir John Parkinson Paul Dudley White
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Paul Dudley White
(1886-1973)
1986
Founder of preventive cardiology
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Original Article
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Original Article, Case III, Intermittent
Pre-excitation
1930
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WPW
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WPW
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UHS pt
WPW
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UHS pt
WPW: Orthodromic AVRT
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WPW and Atrial Fibrillation
(AFib with RVR can be fatal)
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Baseline ECG shows inferior injury and then polymorphic VT
Ischemia with Consequent VT
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Polymorphic VT 10 seconds later
Ischemia with Consequent VT
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Congenital Long QT Syndrome
Three patients with long QT syndrome linked to genetic markers. None were
receiving ß-adrenergic blocking medication. Chromosome 3 mutation in the
cardiac sodium channel gene SCN5A, the QTc in lead II is 570 ms with late-
onset T waves of normal duration and amplitude. Chromosome 7, the QTc in
lead II is 583 ms with low-amplitude T waves. Chromosome 11, the QTc in lead
II is 573 ms with early onset of broad-based T waves.
AHA/ACC Scientific Statement - Evaluation of Syncope.
Circulation 2006:113:316.
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Acquired Long QT interval and Torsades
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Brugada ECG AbnormalityECG changes in the
Brugada syndrome.
ST elevation occurs
in the anterior
precordial leads,
leads V1 and V2.
Type 1 (coved) ECGs
with 1 mV of ST
elevation have the
most prognostic
significance. ECG
recordings may
change over time, as
in this example, and
serial ECGs may be
important.
AHA/ACC Scientific Statement - Evaluation of
Syncope. Circulation 2006:113:316.
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Arrhythmogenic RV
Cardiomyopathy
Kies P et al. Heart
Rhythm 2006;3:225.
Epsilon wave
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Arrhythmogenic RV
Cardiomyopathy
Kenigsberg DN et al. Circulation. 2007;115:e538-e539
Epsilon wave
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Arrhythmogenic RV
Cardiomyopathy
Kenigsberg DN et al. Circulation. 2007;115:e538-e539
RV enlargement and
hyperenhancement of RV
free wall and septum
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ECG in Brugada and RV Cardiomyopathy
RV Cardiomyopathy
Epsilon wave
Brugada pattern
Coved ST elevation
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Evaluation of the Patient:
The “Five-finger” Approach
History
Physical Exam
ECG
Chest X-Ray
Other Tests
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Chest X-Ray in Syncope
• Often not helpful, but important if
cardiac symptoms or signs are present
or if ECG shows hypertrophy or signs of
cardiopulmonary disease
• Cardiomegaly
• Pulmonary hypertension/embolus
• Cardiac calcification (AoV, coronary)
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Evaluation of the Patient:
The “Five-finger” Approach
History
Physical Exam
ECG
Chest X-Ray
Other Tests
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Other Tests in Syncope
Evaluation
Testing should only be done when indicated by findings in the history, physical examination or ECG
• Holter Monitor
• Tilt Table Testing
• Head CT scan
• Cardiac stress test with or without imaging
• Echocardiogram
• Lab tests (hct, BUN)
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Tilt Table
Testing
• Specificity 90%
• Sensitivity 26% to 80%
• In patients with a
negative initial
evaluation and no
evidence of heart
disease, the pretest
probability of
neurocardiogenic
syncope is high, so a
test contributes little to
the diagnosis
Grubb BP. N Engl J Med. 2005;352:1004. Circulation. 2006;113:316.
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Tilt Table
Testing
Grubb BP. N Engl J Med. 2005;352:1004.
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Overview of Common Syncopal
Situations and their Management
• Neurocardiogenic Syncope
• Orthostatic hypotension
• Cardiac Causes
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Neurocardiogenic Syncope
• A syndrome in which “triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia (asystole or relative bradycardia) and peripheral vasodilation.”– “Vasodepressor” (vasodilation)
– “Cardioinhibitory” (bradycardia)
– “Mixed” (both vasodilation and bradycardia)
• Neurocardiogenic syncope is caused by an abnormal or exaggerated autonomic response to various stimuli, of which the most common are standing and emotion.
Chen-Scarabelli C et al. BMJ 2004;329:336.
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Neurocardiogenic Syncope
Differential Diagnosis
• Syncope after cough, micturition, and defecation suggests situational syncope
• Syncope with throat or facial pain (CN IX or VII neuralgia) suggests neurally mediated syncope with neuralgia
• Syncope with pain, fear, or noxious stimuli suggests neurocardiogenic syncope
• Syncope with rotation or turning of the head or neck pressure from shaving, tight collars or neckwear or carotid massage or tumor compression suggests carotid sinus syncope
Chen-Scarabelli C et al. BMJ 2004;329:336.
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Rational Treatment of
Neurocardiogenic Syncope
• Avoid predisposing situations (dehydration,
stress, alcohol consumption, warm
environments, tight clothing)
• Management of anxiety
• Development of coping skills (coping with
precipitating conditions)
• Reassurance that this is a benign condition
• Recognition of presyncopal symptoms
Chen-Scarabelli C et al. BMJ 2004;329:336.
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Physical Countermeasures in
Neurocardiogenic Syncope
• This study was performed in 9 patients with neurogenic orthostatic hypotension, and Valsalva maneuver was avoided; maneuvers continued approximately 45 seconds; biofeedback and 45-minute training sessions were used
• Leg crossing - When standing, cross the right foot over the left and contract the leg musculature
• Toe raise, marching, squat, isometric quadriceps exercise
• Blood pressure increment approximately 20 mmHg
• Patients preferred leg crossing, thigh contraction, toe raise, and squat
Bouvette CM et al. Mayo Clin Proc. 1996;71:847-853 .
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Physical
Countermeasures
in
Neurocardiogenic
Syncope
Krediet CPT et al.
Circulation 2002;106;1684-
1689.
A:
Prodrome B: Start
Countermaneuver
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Physical Countermeasures in
Neurocardiogenic Syncope
• Randomized 14-month follow-up between 110 pts with conventional therapy and 99 pts trained on physical countermeasures (included biofeedback)
Van Dijk N et al. J Am Coll Cardiol. 2006;48:1652-7.
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Pharmacologic Treatment of
Neurocardiogenic Syncope:
(No Agent is Recommended)
• Beta-blockers are rational but ineffective in randomized trials
• Alpha-agonists (midodrine) have been shown to be effective
• Selective serotonin reuptake inhibitors may be effective (1 month, paroxitine in 68 pts)
• Fludrocortisone may be effective
• Disopyramide is not first choice
• Other anticholinergics possible
Chen-Scarabelli C et al. BMJ 2004;329:336.
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Orthostatic Hypotension:
Effects of Aging
• Less HR acceleration (lower parasympathetic tone) and α1-adrenergic vasoconstriction
• Less renal responsiveness to dehydration (with aging: renin, angiotensin and aldosterone lower and natriuretic peptides higher)
• Lower myocardial chamber compliance means greater dependence on ventricular preload and lower tolerance of volume depletion
Gupta V et al. Am J Med. 2007;120:841-847.
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Orthostatic Hypotension
• Definition: SBP fall > 20 mmHg or DBP
fall > 10 mmHg or symptoms of cerebral
hypoperfusion within 1-3 min of
standing
• If the HR increases by 20, it is probably
volume depletion, if <10 it is probably
baroreflex impairment (autonomic
dysfunction)
Gupta V et al. Am J Med. 2007;120:841-847.
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Drugs that Cause Orthostatic
Hypotension
• Alpha-blockers
• Antipsychotics
• Antihypertensives
• Beta-blockers
• Bromocriptine
• Diuretics
• Levadopa
• Marijuana
• Narcotics and sedatives
• Phosphodiesterase – 5
inhibitors
• Tricyclics
• Vasodilators
Gupta V et al. Am J Med. 2007;120:841-847.
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Treatment of Orthostatic Hypotension
• Adjust offending medications
• Arise slowly
• Avoid straining, coughing, prolonged standing in hot weather
• Physical countermeasures
• Raise head of bed 10-20 degrees
• Small meal and coffee in the morning
• Elastic waist high stocking
• Liberalize salt and water intake
• Exercise (swimming, recumbent bike, rowing)
Gupta V et al. Am J Med. 2007;120:841-847.
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Drug Treatment of Orthostatic
Hypotension
Gupta V et al. Am J Med. 2007;120:841-847.
Drug Dose (mg)Contra-
indicationSide Effects
Fludro-
cortisone
Initial 0.1/d
Max 1/d
Hyper-
sensitivity
Supine htn, hypo-
kalemia, HF, HA
Mido-
drine
Initial 2.5 tid
Max 10 tid
Sev OHD, urin
retention, ARF
Supine htn, paresth,
pruritis, piloerection,
Ibuprofen 400-800 tid Sens to NSAID,
bleeding, CRI
GI intol, bleeding,
HA, dizziness, CRI
Caffeine 100-250/da Hyper-
sensitivity
GI irrit, insom, agit,
nervousness
E-poietin* 25-75 U/Kg Uncontr htn Stroke, MI, Htn
*off label
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Syncope due to
Bradyarrhythmias
• Secondary
– to a reversible cause, remove the cause and observe for improvement
– to necessary therapy (e.g., beta-blocker for brady-tachy syndrome or for heart failure or angina), pacemaker is often the preferred option
• Primary (sick sinus syndrome or AV block), pacemaker is generally the preferred option
Sinus node dysfunction
AV node dysfunction
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Pacemaker Therapy in
Neurocardiogenic Syncope
• Not the usual initial treatment
• Dual chamber pacemaker may
relieve symptoms if there is a
large cardioinhibitory
(bradycardia) component
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Syncope due to Tachyarrhythmias
There are many types of tachycardias and many options for therapy, cardiology is often helpful
• Supraventricular tachycardias (less likely to cause syncope) may respond to a radiofrequency ablation procedure (WPW, atrial flutter, others) and pharmacologic therapy
• Most ventricular tachycardias may require a combination of ICD and pharmacologic therapy
• Some ventricular tachycardias occur in a structurally normal heart and may respond to a beta blocker or radiofrequency ablation
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Syncope due to Cardiac
Obstructive Lesion
• Severe aortic stenosis – poor prognosis without surgery, recommend aortic valve replacement (PS, MS also)
• Pulmonary embolism – recommend anticoagulation, consider fibrinolytic therapy or embolectomy for massive or submassive embolism
• Pulmonary hypertension
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Syncope and Neurology
• Asystole occurring in a seizure is rare but not impossible, less rare in temporal seizures
• SUDEP: sudden unexpected death in epilepsy
• Treatment/prevention – meticulous control of seizures; occasionally pacemaker
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Syncope: Indications for Hospitalization
For Diagnosis
• Suspected or known
significant heart disease
• Suspicious ECG
abnormalities
• Syncope during exercise
• Syncope with severe injury
• Family history of SCD
• Palpitations, frequent
symptoms, supine syncope
• High suspicion for cardiac
syncope
For Treatment
• Cardiac arrhythmias
causing syncope
• Syncope due to ischemia
• Syncope due to structural
cardiac or
cardiopulmonary disease
• Neurocardiogenic
syncope requiring
pacemaker
Brignole M. et al. Eur Heart J. 2004;25:2054-72.
ESC Guideline
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Hospitalization for Syncope
Shen WK et al. Circulation. 2004;110:3636-45.
Recommended Consideration Not recommended
(SEEDS)
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Hospitalization for Syncope
• Evidence for heart failure
• Evidence for structural heart disease
• High risk features
– Older age and comorbidities
– ECG ischemia, conduction abnormalities,
or dysrhythmias
– Hematocrit <30 (if obtained)
Huff JS et al. Ann Emerg Med. 2007;49:431-444.
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Brignole M et al.
J Am Coll
Cardiol.
2008;51:284-7.
Hospitalization
for Syncope
From 2004
ESC Guideline
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Syncope
Workup
AHA/ACC Scientific Statement -
Evaluation of Syncope. Circulation
2006:113:316.
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Italian Application of Guidelines in
Urgent Care Setting
• Used a highly structured computerized algorithm based on the 2004 European guidelines; applied to eleven Italian hospitals over a 31-da period (541 pts, 1% of ER visits)
• Hospitals were equipped with full evaluation capabilities including tilt-table, beat-to-beat noninvasive BP, and autonomic function testing as well as the usual facilities
• Computer software suggested diagnoses and recommended tests; an expert was required to provide recommendations to follow the diagnostic workup in 150 (32%) patients
Brignole M. et al. Eur Heart J. 2006;27:76-82.
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Italian
Application of
Guidelines –
Patient
Characteristics
Brignole M. et al. Eur
Heart J. 2006;27:76-82.
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Italian Application of Guidelines –
Patient Flow
Brignole M. et al. Eur Heart J. 2006;27:76-82.
History, Physical, ECG
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Results of Evaluation in Syncope
Brignole M. et al. Eur Heart J. 2006;27:76-82.
CauseInitial
Eval
More
TestsTotal %
Neurally mediated 202 107 309 66
Orthostatic Hypotension 36 10 46 10
Cardiac Arrhythmias 30 23 53 11
Structural Disease 4 17 21 5
Cerebrovascular Dz 0 0 0 0
Unknown 11 2
Non-Syncope 25 25 6
Total (541, 76 dropped out) 272 182 465 100
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Details of Results in Syncope
Brignole M. et al. Eur Heart J. 2006;27:76-82.
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Testing Use in Syncope Evaluation
Brignole M. et al. Eur Heart J. 2006;27:76-82.
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Results of Guideline-Based Management
Brignole M. et al. Eur Heart J. 2006;27:76-82.
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Summary
• Evaluation of syncope: History is the
main diagnostic tool
• Management of syncope
– Hospitalize the high risk patient
– Reassure and educate the low risk patient
• Avoidance of precipitants
• Techniques of physical countermeasures