1. SYNCOPE Mechanisms and Management John Telles MD, FACC August 9, 2006

3. Case Study 20 y/o female competitive cyclist
Dizzy when stands up quickly
Syncope during training ride

4. Syncope (Greek – to interrupt)
Syncope is the sudden transient loss of consciousness and postural tone with spontaneous recovery.
Loss of consciousness occurs within 10 seconds of hypoperfusion of the reticular activating system in the mid brain.

5. Maintenance of Postural Normaltension
Upright posture results in translocation of 30% of central blood volume to dependent body parts within seconds and transcapillary fluid shifts over 30 minutes further reduce blood volume by 5%.
Compensatory responses
Muscle pump
Nuerovascular compensation
Humoral compensation
Local vascular

6. Action of the Musculovenous Pump in Lowering Venous Pressure in the Leg
Bergan J et al. N Engl J Med 2006;355:

7. Maintenance of Postural Normaltension
Neurovascular
Compensation
High pressure
mechanoreceptors
Low pressure mechanoreceptors
The physiology of syncope is depicted graphically in this slide. The afferent trigger signals (eg, pain, emotional upset, dehydration) are not depicted. In the efferent loop of the neural reflex:
Parasympathetic signals from the cerebral cortex reduce heart rate and slow (or block) AV conduction.
Decreased sympathetic activity results in vasodilatation.
Bradycardia and/or hypotension occur.
Carotid baroreceptors and other mechanoreceptors provide paradoxical feedback to the central nervous system, aggravating bradycardia and vasodilatation.
The result may be a downward spiral in heart rate and blood pressure leading to syncope.
Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996.

8. Syncope is important because….
It is common
Costly
May be disabling
May be only warning sign before sudden death

9. Relative Frequency of Syncope
15% of children before the age of 18
16% during 10 year period in men aged
19% during 10 year period in women aged 40 –49
23% during 10 year period in elderly > 70 years old
Recurrence in 35% in 3 years

10. Syncope Mortality Low mortality vs. high mortality
Neurally-mediated syncope vs. syncope with a cardiac cause
Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12): [Framingham Study Population]

11. Syncope: Key questions to address with initial evaluation
Is the loss of consciousness attributable to syncope or not?
Is heart disease present or absent?
Are there important clinical features in the history that suggest the diagnosis?

12. Syncope Mimics Disorders without impairment of consciousness
Falls
Drop attacks
Cataplexy
Psychogenic pseudo-syncope
Transient ischemic attacks
Disorders with loss of consciousness
Metabolic disorders
Epilepsy
Intoxications
Vertebrobasilar transient ischemic attacks

13. Differential Diagnosis of Syncope: Seizures vs Hypotension
Observation
Seizure
Inadequate Perfusion
Onset
Sudden
More gradual
Duration
Minutes
Seconds
Jerks
Frequent
Rare
Headache
Frequent (after)
Occasional (before)
Confusion after
Incontinence
Eye deviation
Horizontal
Vertical (or none)
Tongue biting
Prodrome
Aura
Dizziness
EEG
Often abnormal
Usually normal

14. Unexplained Causes = Approximately 1/3
Causes of True Syncope
Neurally-
Mediated
Orthostatic
Cardiac
Arrhythmia
Structural
Cardio-
Pulmonary 1
VVS
CSS
• Situational
Cough
Post-
Micturition 2
Drug-Induced
• ANS Failure
Primary
Secondary 3
Brady
SN Dysfunction
AV Block
• Tachy VT
SVT
Long QT Syndrome 4
Acute Myocardial Ischemia
Aortic Stenosis
HCM
Pulmonary Hypertension
Aortic Dissection
This slide provides a simple classification of the principal causes of syncope, listed from the most commonly observed (left) to the least common (right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients.
Within the boxes, the most common causes of syncope are indicated for each of the major diagnostic groups.
The terms ‘neurally-mediated syncope’, ‘neurally-mediated reflex syncope,’ and ‘neurocardiogenic syncope’ are generally used synonymously. For purposes of this presentation, ‘neurally-mediated syncope’ is used to define a broad category; ‘neurocardiogenic’ or ‘vasovagal syncope’ refer to a specific condition.
VVS—Vasovagal Syncope
CSS—Carotid Sinus Syndrome
ANS—Autonomic Nervous System
HCM—Hypertrophic Cardiomyopathy
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
Unexplained Causes = Approximately 1/3
DG Benditt, MD. U of M Cardiac Arrhythmia Center

15. Framingham Cohort1 (N=727) Composite Data (Linzer2) (N=1,002)
Causes of Syncope
Framingham Cohort1 (N=727)
Composite Data (Linzer2) (N=1,002)
Cause
Prevalence Mean %
Cause 
Vasovagal 21 18
Orthostatic
9.3 8
Cardiac 10
Seizure
5.2
Neurologic
Medication
6.8 3
Stroke/TIA
4.2
Situational 5
Other
7.8
Carotid Sinus 1
Unknown
35.9 34
There are many causes of syncope—too many to list in this presentation—and new and creative ways to pass out are always possible.
The table on the left provides data on the incidence and prognosis of syncope from the Framingham study. The right shows composite data from five studies. Vasovagal, in any study, represents the most common cause for syncope. This is also referred to as neurocardiogenic syncope. But there are a variety of dysautonomic syndromes that can lead to syncope.
The term ‘vasovagal syncope,’ sometimes referred to as ‘neurocardiogenic syncope,’ encompasses many conditions initiated by an abrupt change in blood pressure and heart rate, heart rate alone, blood pressure alone, or associated with other dysautonomic conditions that lead to the neurocardiogenic reflex. The episode can be situational—witnessing a needle stick—or due to an underlying condition—carotid hypersensitivity, for example.
Cardiovascular causes for syncope include those due to organic heart disease such as aortic stenosis or hypertrophic cardiomyopathy, or due to arrhythmias such as ventricular tachycardia and ventricular fibrillation.
About one-third of patients will never have a cause diagnosed,1,2 and in some studies this number is as much as 50%.3 In these patients, the most likely cause for syncope is benign and is most likely due to a neurocardiogenic reflex.
1 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med. 2002;347(12):
2 Linzer M, Yang E, Estes N, et al. Diagnosing syncope. Ann Intern Med. 1997;126(12):
3Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:
1Soteriades ES, et al. NEJM. 2002;347: Linzer M, et al. Ann Intern Med. 1997;126:

16. Causes of Syncope by Age
Younger Patient
Vasovagal
Situational
Psychiatric
Long QT*
Brugada syndrome*
WPW syndrome*
RV dysplasia*
Hypertrophic cardiomyopathy*
Catecholaminergic VT
Other genetic syndromes
Older Patient
Cardiac**
Mechanical
Arrhythmic
Orthostatic hypotension
Drug-induced
Neurally mediated
Multifactorial
All diagnoses are presumptive unless an episode is observed with documentation of heart rate, blood pressure, cerebral blood flow, EEG activity, etc.
Diagnoses can be categorized by the age of the patient. For patients younger than the age of 40 to 50, there are several benign causes for syndrome. One must, however, be aware of congenital syndromes, such as long QT interval syndrome, Brugada syndrome, WPW syndrome, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and others as possible causes for syncope.
For the older patient, cardiac causes for syncope are common and must be considered seriously. In addition, orthostatic hypotension, while it is benign, can be difficult to treat. Drug-induced causes for syncope include vasodilators, beta blockers, and drugs that lower blood pressure and cause vasodilation in the older patient. This combined with a less robust autonomic nervous system can lead to difficulties with abrupt changes in position and stress. Indeed, many older patients have multifactorial causes for syncope.
Olshansky B. Syncope: Overview and approach to management. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Armonk, NY:Futura Pub Co. 1998:15-71.
Underlined: benign * Rare, not benign ** Not benign .

17. Syncope: Key questions to address with initial evaluation
Is the loss of consciousness attributable to syncope or not?
Is heart disease present or absent?
Are there important clinical features in the history that suggest the diagnosis?

18. Syncope: Important Historical Features
Questions about circumstances just prior to attack
Position (supine, sitting , standing)
Activity (rest, change in posture, during or immediately after exercise, during or immediately after urination, defecation or swallowing)
Predisposing factors (crowded or warm place, prolonged standing post-prandial period) and of precipitating events (fear, intense pain, neck movements)
Questions about onset of the attack
Nausea, vomiting, feeling cold, sweating, pain in chest, pain in neck, or shoulders,

19. Syncope: Important Historical Features
Questions about onset of the attack
Nausea, vomiting, feeling cold, sweating, pain in chest, pain in neck, or shoulders,

20. Syncope: Important Historical Features
Questions about attack (eye witness)
Skin color (pallor, cyanotic)
Duration of loss of consciousness
Movements ( tonic-clonic, etc.)
Tongue biting
Questions about the end of the attack
Nausea, vomiting, diaphoresis, feeling cold, muscle aches, confusion, skin color, wounds

21. Syncope: Important Historical Feature
Questions about background
Number and duration of syncope spells
Family history of arrhythmic disease or sudden death
Presence of cardiac disease
Neurological disease (Parkinsons, epilepsy, narcolepsy)
Internal history (Diabetes)
Medications (Hypotensive, negative chronotropic and antidepressant agents)

22. Clinical Features Suggesting Specific Cause of Syncope
Neurally-Mediated Syncope
Absence of cardiac disease
Long history of syncope
After sudden unexpected, unpleasant sensation
Prolonged standing in crowded, hot places
Nausea vomiting associated with syncope
During or after a meal
With head rotation or pressure on carotid sinus
After exertion

23. Clinical Features Suggesting Specific Cause of Syncope
Syncope due to orthostatic hypotension
After standing up
Temporal relationship to taking a medication that can cause hypotension
Prolonged standing
Presence of autonomic neuropathy
After exertion

24. Clinical Features Suggestion Cause of Syncope
Cardiac Syncope
Presence of structural heart disease
With exertion or supine
Preceded by palpitations
Family history of sudden death

25. Initial Exam: Thorough Physical
Vital signs
Heart rate
Orthostatic blood pressure change
Cardiovascular exam: Is heart disease present?
ECG: Long QT, pre-excitation, conduction system disease
Echo: LV function, valve status, HCM
Neurological exam
Carotid sinus massage
Perform under clinically appropriate conditions preferably during head-up tilt test
Monitor both ECG and BP
HCM—Hypertrophic Cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

26. Carotid Sinus Massage (CSM)
Absolute contraindications2
Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
Complications
Primarily neurological
Less than 0.2%3
Usually transient
Method1
Massage, 5-10 seconds
Don’t occlude
Supine and upright posture (on tilt table)
Outcome
3 second asystole and/or mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome
Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here1 has proven both safe and effective.
Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
1Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000;83:
2Linzer M, Yang EH, Estes M, et al. Diagnosing Syncope: Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):
3Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

27. Syncope: Diagnostic Testing in Hospital Strongly Recommended
Suspected/known ‘significant’ heart disease
ECG abnormalities suggesting potential life-threatening arrhythmic cause
Syncope during exercise
Severe injury or accident
Family history of premature sudden death
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

28. Diagnostic Methods and Yields
Procedure
History and Physical Exam
Yield*
25-35%1
ECG
2-11%2
Monitoring
Holter Monitoring
2%3
External Loop Recorder
20% 3
Insertable Loop Recorder
43-88%4,5,6
Test/Procedure
Tilt Table
11-87% 1,7
EP Study without SHD**
11% 8
EP Study with SHD
49% 1
Current testing modalities are limited in terms of ability to capture infrequent events, patient compliance, and diagnostic yield.9
Diagnostic yield is defined as the number of patients with diagnostically positive test results, divided by the number of patients tested. Or, in the case of monitoring studies, the sum of true-positive and true-negative test results divided by the number of patients tested (Linzer M, et al. Ann Intern Med. 1997;126(12): ).
Due to the complex diagnosis of syncope, patients may undergo extensive investigations which are often low-yield, expensive, and/or invasive.1 And when inconclusive, these tests are often repeated.9
These are the more typical diagnostic tests.
1Kapoor W. Medicine. 1990;69(3):
2Kapoor W. Am J Med. 1991;90:
3Krahn AD, Klein GJ, Yee R. Cardiol Clin.1997;15(2):
4Krahn AD, Klein GJ, Yee R, Norris C. Am J Cardiol. 1998;82:
5Krahn AD, Klein GJ, Yee R, et al. Circulation. 1999;99:
6Krahn AD, Klein GJ, Yee R, et al. JACC. 2003;42:
7Kapoor W. JAMA. 1992;268:
8Linzer M, Yang B, Estes M, et al. Ann Intern Med. 1997;127:76-86.
9Olshansky, B. Syncope: Overview and approach to management. In: Olshansky B and Grubb B, eds. Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co;1998:15-71.
**Structural Heart Disease

29. Heart Monitoring Options
12-Lead
10 Seconds
2 Days
Holter Monitor
Event Recorders (non-lead and loop)
7-30 Days
Up to 14 Months
ILR
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6: 1 2 3 4 5 6 7 8 9 10 11 12 13 14
TIME (Months)

30. Insertable Loop Recorder (ILR)
The ILR is an implantable patient – and automatically – activated monitoring system that records subcutaneous ECG and is indicated for:
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia

31. Symptom-Rhythm Correlation with the ILR
These are examples of ECG recordings obtained by the Reveal® ILR system in two symptomatic patients.
The gold standard for determining if a syncope episode may be due to an arrhythmia is to record the rhythm during symptoms, i.e., symptom-rhythm correlation. The ILR may help rule-in or rule-out arrhythmogenic causes.
These strips depict findings from an ILR interrogation as they appear on the programmer screen. In order to view the event in greater detail, one taps the screen over the ECG of interest.
On-screen calipers are available at every zoom level to measure cycle length in milliseconds or beats per minute.
Note that the ‘A’ represents an auto-activated event; the ‘P’ indicates when the patient activated the device.
Left strip: Infra-Hisian AV block: dual chamber pacemaker.
Right strip: VT and VF: ICD, meds.
Medtronic data on file.
CASE: 56 year-old woman with refractory syncope accompanied with seizures.
CASE: 65 year-old man with syncope accompanied by brief retrograde amnesia.
Medtronic data on file.

32. Head-Up Tilt Test (HUT)
60° - 80°
Protocols vary
Useful as diagnostic adjunct in atypical syncope cases
Useful in teaching patients to recognize prodromal symptoms
Not useful in assessing treatment
The rationale for undertaking tilt table testing in patients suspected of having vasovagal (VVS) syncope is summarized here. The test may provide useful diagnostic information and also an opportunity for patients to become more familiar with the condition and its possible warning signs.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

33. Response to Tilt Table Testing
Normal Vasal vagal

34. Response to Tilt Table Testing
POTS Dysautonomia

35. Indication for Tilt Table Testing
The evaluation of recurrent syncope, or a single syncopal event accompanied by physical injury, motor vehicle accident, or in high risk setting in which clinical features suggest vasovagal
In patients in whom dysautonomias may contribute to symptomatic hypotension
Evaluation of recurrent exercise induced syncope in patients without structural heart disease

36. Conventional EP Testing in Syncope
Greater diagnostic value in older patients or those with SHD
Less diagnostic value in healthy patients without SHD
Useful diagnostic observations:
Inducible monomorphic VT
SNRT > 3000 ms or CSNRT > 600 ms
Inducible SVT with hypotension
HV interval ≥ 100 ms (especially in absence of inducible VT)
Pacing induced infra-nodal block
Conventional EP testing (i.e., electrical stimulation without autonomic studies such as HUT) has not been highly effective in substantiating a basis for syncope. In this regard, EPS has been more effective in patients with structural cardiovascular disease than in those with normal cardiovascular status.
The most important findings at EPS in regard to the evaluation of syncope patients are listed in this slide.
SHD—Structural Heart Disease
SNRT—Sinus Node Recovery Time
CSNRT—Corrected Sinus Node Recovery Time
Benditt D. Syncope. In: Topol E, ed. Textbook of Cardiovascular Medicine. Philadelphia, PA: Lippencott Williams & Wilkins;2002:
Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

37. Diagnostic Limitations of EPS
Difficult to correlate spontaneous events and laboratory findings
Positive findings1
Without SHD: 6-17%
With SHD: 25-71%
Less effective in assessing bradyarrhythmias than tachyarrhythmias2
EPS findings must be consistent with clinical history
Beware of false positive
*SHD—Structural Heart Disease
1Linzer M, Yang E, Estes M, et al. Diagnosing Syncope. Part 2: Unexplained Syncope. Ann Int Med. 1997;127:76-86.
2Lu F and Bergfeldt L. Role of electrophysiologic testing in the syncope evaluation. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;80-95.

38. “…cardiac syncope can be a harbinger of sudden death.”
Survival with and without syncope
6-month mortality rate of greater than 10%
Cardiac syncope doubled the risk of death
Includes cardiac arrhythmias and SHD
No Syncope
Vasovagal and Other Causes
Cardiac Cause
Follow-Up (yr)
Probability of Survival
1.0
0.8
0.6
0.4
0.2
0.0
Cardiac causes include both arrhythmias and structural heart problems, both of which contribute to high mortality rates. One of the goals, therefore, is to attempt to either rule out or rule in arrhythmic disorders.
The statistic of a 1-year mortality rate ranging from 18-33% was validated in the September 19th, 2002 issue of the New England Journal of Medicine. The incidence and prognosis of syncope was studied in more than 7,800 participants in the Framingham Heart Study from 1971 to 1998.
The study found a 6-month mortality rate of greater than 10%.1
Cardiac syncope doubled the risk of death .1
Syncope of unknown cause was the largest category of causes.2
50% of syncope cases could not be diagnosed after conventional evaluation of detailed history, physical exam, and ECG.3
Because the precise cause of syncope is identified in fewer than half the patients during initial evaluation, the challenge lies in identifying those at high risk for death.
Cardiac syncope is not benign.
1 Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope. N Engl J Med ;347(12):
2 Kapoor WN. Evaluation and outcome of patients with syncope. Medicine. 1990;69:
3 Linzer M, Yang E, Estes N, et al. Diagnosing syncope. Ann Intern Med. 1997;126(12):
Soteriades ES, et al. N Engl J Med. 2002;347:878.

39. Syncope Due to Cardiac Arrhythmias
Bradyarrhythmias
Sinus arrest, exit block
High grade or acute complete AV block
Can be accompanied by vasodilatation (VVS, CSS)
Tachyarrhythmias
Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome)
Paroxysmal SVT or VT
Torsade de pointes
Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

40. Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms
Acute MI/Ischemia
2° neural reflex bradycardia
Vasodilatation, arrhythmias, low output (rare)
Hypertrophic cardiomyopathy
Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex
Acute aortic dissection
Neural reflex mechanism, pericardial tamponade
Pulmonary embolus/ pulmonary hypertension
Neural reflex, inadequate flow with exertion
Valvular abnormalities
Aortic stenosis – Limited output, neural reflex dilation in periphery
Mitral stenosis, atrial myxoma – Obstruction to adequate flow
This slide lists important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope.
Obstruction of blood flow and arrhythmias are often the mechanisms for the syncope; all are high risk.
The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
MI—myocardial infarction
HCM—hypertrophic cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

41. Neurally-Mediated Reflex Syncope
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Situational syncope
Post-micturition
Cough
Swallow
Defecation
Blood drawing, etc.
The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation.
Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur occasionally and are usually recognized only if a detailed medical history is obtained.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6: .

42. VVS Clinical Pathophysiology
Neurally-mediated physiologic reflex mechanism with two components:
1. Cardioinhibitory (↓ HR)
2. Vasodepressor (↓ BP) despite heart beats, no significant BP generated
Both components are usually present 1
Vasovagal syncope, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow.
Hypotension is the result of two pathophysiologic components:
Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature)
Vasodilatation
The relative contribution of these two components varies among patients.
Wieling W, Gert van Dijk J, van Lieshout J, Benditt D. Pathophysiology and clinical presentation. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003;11-22. 2

43. VVS Incidence Most common form of syncope
8% to 37% (mean 18%) of syncope cases
Depends on population sampled
Young without SHD, ↑ incidence
Older with SHD, ↓ incidence
The incidence of vasovagal syncope is poorly known.
The published data that exists mostly dates from before the advent of tilt table testing.
Linzer surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope.
Standards for diagnosis and reporting are still emerging.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):

44. VVS General Treatment Measures
Long-term prevention
Tilt training
Education
Diet, fluids, salt
Support hose
Drug therapy
Pacing
Optimal treatment strategies for VVS are a source of debate
Treatment goals
Acute intervention
Physical maneuvers, eg, crossing legs or tugging arms
Lowering head
Lying down
Optimal management strategies for VVS are a source of debate. Long-term prevention measures include:
Patient education, reassurance, and instruction.
Control of fluids, salt, and diet may help reduce incidence.
Support hose may limit blood pooling in the legs and feet.
Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date
Pacing may benefit some patients. Subsequent slides will examine the utility of pacing in very symptomatic VVS patients.
When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. This might include physical maneuvers such as crossing the legs, lowering the head, or lying down.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

45. CSS Carotid Sinus Syndrome
Syncope clearly associated with carotid sinus stimulation is rare (≤1% of syncope)
CSS may be an important cause of unexplained syncope/falls in older individuals
Prevalence higher than previously believed
Carotid Sinus Hypersensitivity (CSH)
No symptoms
No treatment
Carotid sinus syndrome (CSS) is an important and often overlooked cause of syncope, and in addition is believed to be a frequent cause of unexplained falls in older individuals. The underlying cause of CSS is considered to be a hypersensitive carotid sinus. Carotid Sinus Hypersensitivity (CSH) is diagnosed by using Carotid Sinus Massage (CSM). The method of carotid sinus massage, and the findings diagnostic of CSS were presented on previous slides.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Sutton R. Carotid sinus syndrome: clinical presentation, epidemiology, and natural history. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:138.

46. CSS Etiology
Sensory nerve endings in the carotid sinus walls respond to deformation
Previous neck surgery may contribute
Increased afferent signals to brain stem
Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation
Carotid Sinus
The etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles.
Sensory nerve endings in the carotid sinus walls respond to deformation.
An increase in afferent traffic results in cardioinhibition and vasodilatation.
Deafferentation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.
Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:25-29.
Kenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the Older Patient. Kenny RA ed. London: Chapman & Hall Medical; 1996:

47. SAFE PACE Syncope And Falls in the Elderly – Pacing And Carotid Sinus Evaluation
Objective
Determine whether cardiac pacing reduces falls in older adults with carotid sinus hypersensitivity
Randomized controlled trial (N=175)
Adults > 50 years, non-accidental fall, positive CSM
Pacing (n=87) vs. No Pacing (n=88)
Results
More than 1/3 of adults over 50 years presented to the Emergency Department because of a falls have CS hypersensitivity
With pacing, falls  70%
Syncopal events  53%
Injurious events  70%
The study was a randomized controlled trial, pacing versus no pacing, performed at the Royal Victoria Infirmary in Newcastle, between April 1998 and May Patients were followed for 12 months after randomization.
The inclusion criteria were consecutive adults, over the age of 50 years, presenting with a non-accidental fall, who exhibited a positive response to CSM and who had no evidence of cognitive impairment or dementia.
In patients with unexplained falls and a diagnosis of cardioinhibitory carotid sinus hypersensitivity, cardiac pacing reduced the total number of falls by 70%, total syncopal events by 53%, and total injurious events by 70%.
There was a statistically significant reduction in the total number of falls among the pacemaker patient group, with a 70% reduction in total falls compared with the control group.
Only 28 patients reported syncope; 22 syncopal events were reported by paced patients and 47 by controls. Although there was a 50% reduction in the overall number of syncopal episodes, this did not reach statistical significance.
There was also a 70% reduction in the total number of injury events, from 202 in the control group to 61 in paced patients.
Kenny RA, Richardson D, Steen N, et al. Carotid sinus syndrome: A modifiable risk factor for nonaccidental falls in older adults (SAFE PACE). J Am Coll Cardiol. 2001;38:
Kenny RA. J Am Coll Cardiol. 2001;38:

48. Orthostatic Hypotension
Secondary autonomic failure
Diabetes
Alcohol
Amyloid
Etiology
Drug-induced (very common)
Diuretics
Vasodilators
Primary autonomic failure
Multiple system atrophy
Parkinson’s Disease
Postural Orthostatic Tachycardia Syndrome (POTS)
Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions.
The most important conditions predisposing to orthostatic syncope are listed here.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

49. Treatment Strategies for Orthostatic Intolerance
Patient education, injury avoidance
Hydration
Fluids, salt, diet
Minimize caffeine/alcohol
Sleeping with head of bed elevated
Tilt training, leg crossing, arm pull
Support hose
Drug therapies
Fludrocortisone, midodrine, erythropoietin
Tachy-Pacing (probably not useful)
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:

50. Syncope and Driving
“I want to die peacefully in my sleep like my grandfather did, not like the screaming passengers in his car.”
George Burns

51. Syncope and Driving: Medical-Legal Concerns
State of California requires physicians to report, in good faith, patients who have a physical or mental condition which, in the physician’s judgment, impairs the patient’s ability to exercise reasonable and ordinary control over a motor vehicle. The report may be made without the patient’s informed consent.
The physician is obliged to inform the patient of the severity of the condition and that operating a motor vehicle is advised against. This informed advise should be documented in the medical record.

52. Syncope and Driving: Medical Legal Concerns
Examples of syncopal conditions that would prohibit driving
Untreated syncope in patients with heart disease
Undiagnosed recurrent syncope which occurs without prodrome and can occur while sitting

53. 20 y/o female cyclist, dizzy when stands quickly, syncope during training ride

54. 20 y/o female cyclist, dizzy when stands quickly, snycope during training ride
Sitting: HR 65, BP 120/80 , Standing: HR 90, BP 115/80
EKG normal

55. 20 y/o female cyclist, dizzy with standing quickly, syncope on training ride
Sitting: HR 65, BP 120/80 Standing: HR 90, BP 115/80
EKG normal
Echo normal

56. 20 y/o female cyclist, dizzy when stands quickly, syncope during training ride
Sitting:HR 65, BP 120/80, Standing HR 90, BP 115/80
EKG normal
Echo normal
Exercise test normal

57. 20 y/o female cyclist
Dizzy when stands quickly, syncope during training ride
Sitting: HR 65, BP 120/80, Standing: HR 90 BP 115/80
EKG normal
Echo normal
Exercise test normal
Tilt test abnormal

58. Diagnosis Treatment Postural orthostatic tachycardia syndrome POTS
hydration
fludrocortisone
midodrine
welbutrin
zoloft
procrit HS

59. Diagnostic Objectives
Distinguish true syncope from syncope mimics
Determine presence of heart disease and risk for sudden death
Establish the cause of syncope with sufficient certainty to:
Assess prognosis confidently
Initiate effective preventive treatment

60. How to Evaluate Syncope
History: Patient and witnesses
Physical: Including carotid massage and ECG Rx
Neurocardiogenic cause?
No obvious cause?
No heart disease?
Transient or
reversible cause?
Suspected cardiac or arrhythmic cause?
yes
yes
yes
yes
No work-up or
chronic therapy
Admit, cardiology
consult, EPS*
No Rx
1st episode?
There is a valid approach to assessing patients with syncope. The most crucial aspect is to obtain a careful history from the patient, family, and witnesses. Based on the history and physical exam, a plan can be developed. There may be a transient or reversible cause for syncope and the problem can be easily solved with no further work-up or chronic therapy. If there is a suspected cardiac cause for syncope or an arrhythmic cause for syncope, hospital admission must be considered as well as an electrophysiology consult. An electrophysiologic study may be useful in the patient with a bundle branch block or a moderately impaired ejection fraction.
For neurocardiogenic syncope, if it is clear that this is the potential etiology with no obvious trigger and no heart disease, no admission is required. If it is the first episode, no therapy is required. If recurrent episodes occur without obvious trigger, a tilt table test might be useful. Further, in patients with recurrent syncope, an external loop recorder is useful and should be considered before a tilt table test if palpitations are associated with syncope. If a diagnosis cannot be made in or out of the hospital, then an implantable loop recorder may be useful to help make the diagnosis.
Olshansky, B. Syncope: Overview and approach to management. In: Olshansky B and Grubb B, eds. Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co;1998:15-71. no +
Tilt table Rx Rx + + - - +
Loop recorder Rx -
*EPS if BBB or LVEF < 40%
Referral
Olshansky B. Syncope: Mechanisms and Management. Futura Pub. Co