Syncope

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

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 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)

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)

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 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 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 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

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 >30 bpm increase in heart rate Heart increases to > 120 bpm (in first 10 minutes)

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 >30 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

27. Therapeutic Approach 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)

28. Therapeutic Approach 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.