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Title:

Syncope

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Bradycardia. Tachycardia. Aortic Stenosis. Aortic dissection. Hypertrophic cardiomyopathy ... sinus is thought to 'mimic' hypertension leading to bradycardia ... – PowerPoint PPT presentation

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Title: Syncope


1
Syncope
  • Wm. W. Barrington MD FACC
  • Associate Professor of Medicine
  • University of Pittsburgh Medical Center

PaACC Fellows in Training Program May 2008
2
What is syncope?
  • Sudden, temporary loss of consciousness
    associated with the inability to maintain
    postural tone, followed by spontaneous recovery.
  • Also referred to as
  • Fainting
  • Passing out

3
Syncope
Significant Medical Problem
  • Affects 1 million Americans each year. (1)
  • Accounts for 3 of ED visits and 6 of hospital
    admissions. (1)
  • Prevalence of syncope in general population is
    between 15 and 40. (2)
  • 39 of medical students have passed out at
    least once. (2)

1. Shukla GJ and Zimetbaum PJ Circulation (2006)
113 715-17 2. Sheldon RS, Sheldon AG, Connolly
SJ et al J Cardiovasculatr Electrophysiology
(2006) 17 49-54.
4
Etiology
5
Etiology
  • Cardiac
  • Bradycardia
  • Tachycardia
  • Aortic Stenosis
  • Aortic dissection
  • Hypertrophic cardiomyopathy
  • Long QT Syndrome
  • Unknown
  • ? Unknown
  • We will focus today on the noncardiac causes of
    syncope.

6
Etiology (3)
X
3. Grubb B Circulation (2005) 1112997-3006
7
Reflex syncope is a sudden failure of the
autonomic nervous system (ANS) to maintain
adequate vascular tone during orthostatic stress
8
(No Transcript)
9
Neurocardiogenic Syncope
  • Typically occurs in younger patients and has 3
    distinct phases
  • Prodrome of lightheadedness, diaphoresis, nausea
  • Sudden loss of consciousness (LOC)
  • Rapid recovery
  • In older patients, prodromal symptoms less
    common, but LOC still sudden

10
Neurocardiogenic Syncope
Evaluation of Neurocardiogenic Syncope
  • A comprehensive history and physical is the most
    important aspect of the evaluation
  • Supine, sitting and upright blood pressures may
    be helpful
  • Head up Tilt Table (HUTT) testing is often
    employed to confirm or establish the diagnosis

11
Neurocardiogenic Syncope
Head up Tilt Table (HUTT) testing is a method of
examining the effect of the autonomic nervous
system on heart rate and BP
  • 60 to 70 HUTT removes the effect of the lower
    extremity muscle pump
  • Consciousness is thus maintained by appropriate
    interaction of the sympathetic and
    parasympathetic limbs of the ANS

12
Neurocardiogenic Syncope
Head up Tilt Table (HUTT) testing
  • Specificity 90 (without provocation)
  • Short term reproducibility is 80 to 90
  • Individuals with NCS demonstrate a sudden drop
    in BP that is frequently followed by a drop in
    heart rate
  • Commonly, we see one of 3 abnormal responses

13
Vasodepressor Response
14
30 bpm
Continuous recording
60 bpm
Syncope
18 bpm
After 15 minutes of HUTT testing
15
Mixed Vasodepressor/Cardioinhibitory Response
16
Continuous recording
20 bpm
Asystole
7 minutes of HUTT testing
17
Cardioinhibitory Response
18
Situational Syncope
  • Syncope that occurs under a specific set of
    circumstances
  • Micturition
  • Defecation
  • Cough
  • Patients are typically free of symptoms at other
    times
  • Sudden activation of mechanoreceptors at an
    affected site may activate the ANS leading to
    hemodynamic collapse

19
Carotid Sinus Hypersensitivity
  • Pressure on the carotid sinus is thought to
    mimic hypertension leading to bradycardia
  • The symptoms are very similar to those seen with
    NCS

20
Postural Orthostatic Tachycardia Syncope (POTS)
  • Hallmark of syndrome is persistent tachycardia
    while upright
  • Severe fatigue
  • Exercise intolerance
  • Palpitations
  • Syncope and near syncope

21
Postural Orthostatic Tachycardia Syncope (POTS)
  • Pathophysiology appears to be failure of
    peripheral vascular resistance to increase in
    the face of orthostatic stress, thus the heart
    rate and inotropic state increase to compensate.
  • Tilt Table Testing
  • gt30 bpm increase in heart rate
  • Heart increases to gt 120 bpm (in first 10 minutes)

22
POTS Response
23
Therapeutic Approach
  • Avoid precipitating circumstances
  • Dehydration
  • Extreme heat
  • Increase Fluid intake (possibly salt)
  • Lay or sit down when prodromal symptoms begin
  • Encourage moderate aerobic and isometric exercise

24
Therapeutic Approach
  • Tilt table training may be helpful
  • Elastic support hose (effective if waist high
    and provide gt30 mm Hg ankle pressure)
  • Elevation of head of bed
  • Isometric counter maneuvers such as leg or arm
    tensing may abort episodes that are detected
    early.
  • Many individuals finally need pharmacotherapy

25
From Grubb B Circulation (2005) 1112997-3006
26
Fluids/salt Stockings Fludrocortisone
Selective serotonin Re-uptake inhibitors
Midodrine
Anticholenergics
Beta blockers Disopyramide
27
Therapeutic Approach
Is there a role for cardiac pacing?
  • Early studies showed single chamber VVI pacing
    was ineffective.
  • Original, non-blinded studies showed a benefit
    with dual chamber pacing
  • Two recent randomized, blinded studies failed to
    show a benefit with pacing
  • Vasovagal Pacemaker Study (VPS) II (4)
  • Vasovagal Syncope and Pacing Trial (5)

4. Connolly sj et al JAMA (2003) 2892224-9
5.Raviele A et al European Heart Journal
(2004)251741-48
28
Therapeutic Approach
Cardiac pacing is not routinely first line
therapy.
  • In patients with recurrent syncope where no
    other therapy is effective, pacing may have a
    role in reducing the frequency of syncope or
    prolonging the time from onset of symptoms to
    frank syncope, allowing the patient to avoid
    injury.

29
Thank you for your attention.I would be happy
to take any questions.
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